Anti-C1q antibodies: a biomarker for diagnosis and management of lupus nephritis. A narrative review.

Nephritis is a frequent and severe complication of Systemic Lupus Erythematous (SLE). The clinical course of lupus nephritis (LN) is usually characterized by alternating phases of remission and exacerbation. Flares of LN can lead to deterioration of kidney function, necessitating timely diagnosis and therapy. The presence of autoantibodies against C1q (anti-C1qAb) in the sera of SLE patients has been reported in various studies. Some research suggests that the presence and changes in the titer of anti-C1qAb may be associated with the development of LN, as well as with LN activity and renal flares. However, the exact role of anti-C1qAb in LN remains a subject of debate. Despite variability in the results of published studies, anti-C1qAb hold promise as noninvasive markers for assessing LN activity in SLE patients. Measuring anti-C1qAb levels could aid in diagnosing and managing LN during periods of both inactive disease and renal flares. Nevertheless, larger controlled trials with standardized laboratory assays are necessary to further establish the utility of anti-C1qAb in predicting the reactivation and remission of LN and guiding treatment strategies.

Urticarial Vasculitis.

Urticarial vasculitis is a rare autoimmune disorder characterized by persistent edematous papules and plaques on the skin that last longer than 24 hours, often accompanied by systemic symptoms such as joint pain and fever. Unlike common urticaria, this condition involves inflammation of small blood vessels, leading to more severe and long-lasting skin lesions with a tendency to leave a bruiselike appearance. Diagnosis is challenging and may require a skin biopsy. Associated with underlying autoimmune diseases, treatment involves managing symptoms with medications such as antihistamines and corticosteroids, addressing the immune system's dysfunction, and treating any concurrent autoimmune conditions.

Clinical Relevance of Anti-C3 and Anti-C4 Autoantibodies in Lupus Nephritis.

Introduction: Complement system overactivation is pivotal in lupus nephritis (LN) pathophysiology. Considering that anti-C3 autoantibodies play a significant role in LN pathophysiology, we explored them as disease activity biomarkers and compared them to the ones against the homologous protein, C4. Methods: We investigated the presence of anti-C3 and anti-C4 IgG autoantibodies in a LN cohort (N = 85 patients) and monitored their changes over time. We correlated autoantibody presence with clinical parameters. We conducted cross-sectional and longitudinal analyses (N = 295 samples, 8 years follow-up) to explore associations between autoantibodies and disease progression. Antigen-specific anti-C3 or anti-C4 IgG were purified from plasma by affinity chromatography and their reactivity was tested for cross-reactivity against purified C3 or C4 by enzyme-linked immunosorbent assay (ELISA). Results: The reactivity against C3 was independent of C4. Our study revealed distinct roles for anti-C3 and anti-C4 in LN. Anti-C3 IgG exhibited stronger clinical correlations than anti-C4, showing associations with hypocomplementemia, anti-dsDNA, class IV LN, and active disease according to British Isles Lupus Assessment Group (BILAG) renal score. In a longitudinal analysis, anti-C3 positivity at initial sampling predicted present and future disease exacerbation alone and even better when combined with anti-dsDNA, as indicated by a transition to BILAG category A. Conclusion: Our research provides insights into anti-C3/C3b and anti-C4 autoantibodies in LN, revealing that they are often not cross-reactive. Anti-C3 utility as disease activity biomarkers is underscored by its stronger clinical associations and predictive value for future flares. Combining anti-C3 and anti-dsDNA out-performs the 2 factors alone, suggesting that the incorporation of anti-C3/C3b quantification into routine clinical practice could improve LN management.

[Laboratory diagnostics for vasculitis beyond antineutrophil cytoplasmatic autoantibodies]. / Labordiagnostik bei Vaskulitiden jenseits von antineutrophilen zytoplasmatischen Autoantikörpern.

The diagnosis of systemic vasculitis (SV) is a major clinical challenge due to the very different forms of presentation and requires an interdisciplinary approach. Targeted laboratory diagnostics support making the diagnosis, differential diagnosis and classification and are also a key component in the detection of active organ manifestations and treatment complications. The basic laboratory tests include the erythrocyte sedimentation rate (ESR), C­reactive protein (CRP), blood count, serum creatinine, urinalysis, specific autoantibodies, complement, immunoglobulins, cryoglobulins and hepatitis B and C serology. Antineutrophil cytoplasmic autoantibodies (ANCA), antiglomerular basement membrane antibodies (anti-GBM antibodies) and anti-C1q antibodies are valuable laboratory markers for the diagnosis of the various forms of small vessel vasculitis. There are no specific laboratory tests for the diagnosis of medium and large vessel vasculitis. Despite advances in our understanding of the pathogenesis of vasculitis, no biomarkers have yet been identified that can be reliably used to guide treatment or that are useful in distinguishing vasculitis from other inflammatory diseases such as infections or treatment complications.

A critical view on autoantibodies in lupus nephritis: Concrete knowledge based on evidence.

Deposition of autoantibodies in glomeruli is a key factor in the development of lupus nephritis (LN). For a long time, anti-dsDNA and anti-C1q antibodies were thought to be the main cause of the kidney damage. However, recent studies have shown that the list of autoantibidies that have renal tropism and deposit in the kidney in LN is increasing and the link between anti-dsDNA and renal pathology is weak due to potential confounders. Aspecific bindings of dsDNA with cationic antibodies and of anti-dsDNA with several renal antigens such as actinin, laminin, entactin, and annexinA2 raised doubts about the specific target of these antibodies in the kidney. Moreover, the isotype of anti-dsDNA in SLE and LN has never received adequate interest until the recent observation that IgG2 are preponderant over IgG1, IgG3 and IgG4. Based on the above background, recent studies investigated the involvement of anti-dsDNA IgG2 and of other antibodies in LN. It was concluded that circulating anti-dsDNA IgG2 levels do not distinguish between LN versus non-renal SLE, and, in patients with LN, their levels do not change over time. Circulating levels of other antibodies such as anti-ENO1 and anti-H2 IgG2 were, instead, higher in LN vs non-renal SLE at the time of diagnosis and decreased following therapies. Finally, new classes of renal antibodies that potentially modify the anti-inflammatory response in the kidney are emerging as new co-actors in the pathogenetic scenario. They have been defined as 'second wave antibodies' for the link with detoxifying mechanisms limiting the oxidative stress in glomeruli that are classically stimulated in a second phase of inflammation. These findings have important clinical implications that may modify the laboratory approach to LN. Serum levels of anti-ENO1 and anti-H2 IgG2 should be measured in the follow up of patients for designing the length of therapies and identify those patients who respond to treatments. Anti-SOD2 could help to monitor and potentiate the anti-inflammatory response in the kidney.

In vivo evaluation of Clostridioides difficile enoyl-ACP reductase II (FabK) inhibition by phenylimidazole unveils a promising narrow-spectrum antimicrobial strategy.

Clostridioides difficile infection (CDI) is a leading cause of hospital-acquired diarrhea, which often stems from disruption of the gut microbiota by broad-spectrum antibiotics. The increasing prevalence of antibiotic-resistant C. difficile strains, combined with disappointing clinical trial results for recent antibiotic candidates, underscores the urgent need for novel CDI antibiotics. To this end, we investigated C. difficile enoyl ACP reductase (CdFabK), a crucial enzyme in de novo fatty acid synthesis, as a drug target for microbiome-sparing antibiotics. To test this concept, we evaluated the efficacy and in vivo spectrum of activity of the phenylimidazole analog 296, which is validated to inhibit intracellular CdFabK. Against major CDI-associated ribotypes 296 had an Minimum inhibitory concentration (MIC90) of 2 µg/mL, which was comparable to vancomycin (1 µg/mL), a standard of care antibiotic. In addition, 296 achieved high colonic concentrations and displayed dosed-dependent efficacy in mice with colitis CDI. Mice that were given 296 retained colonization resistance to C. difficile and had microbiomes that resembled the untreated mice. Conversely, both vancomycin and fidaxomicin induced significant changes to mice microbiomes, in a manner consistent with prior reports. CdFabK, therefore, represents a potential target for microbiome-sparing CDI antibiotics, with phenylimidazoles providing a good chemical starting point for designing such agents.

Human anti-C1q autoantibodies bind specifically to solid-phase C1q and enhance phagocytosis but not complement activation.

Autoantibodies directed against complement component C1q are commonly associated with autoimmune diseases, especially systemic lupus erythematosus. Importantly, these anti-C1q autoantibodies are specific for ligand-bound, solid-phase C1q and do not bind to fluid-phase C1q. In patients with anti-C1q, C1q levels are in the normal range, and the autoantibodies are thus not depleting. To study these human anti-C1q autoantibodies at the molecular level, we isolated C1q-reactive B cells and recombinantly produced nine monoclonal antibodies (mAbs) from four different healthy individuals. The isolated mAbs were of the IgG isotype, contained extensively mutated variable domains, and showed high affinity to the collagen-like region of C1q. The anti-C1q mAbs exclusively bound solid-phase C1q in complex with its natural ligands, including immobilized or antigen-bound IgG, IgM or CRP, and necrotic cells. Competition experiments reveal that at least 2 epitopes, also targeted by anti-C1q antibodies in sera from SLE patients, are recognized. Electron microscopy with hexameric IgG-C1q immune complexes demonstrated that multiple mAbs can interact with a single C1q molecule and identified the region of C1q targeted by these mAbs. The opsonization of immune complexes with anti-C1q greatly enhanced Fc-receptor-mediated phagocytosis but did not increase complement activation. We conclude that human anti-C1q autoantibodies specifically bind neo-epitopes on solid-phase C1q, which results in an increase in Fc-receptor-mediated effector functions that may potentially contribute to autoimmune disease immunopathology.

Anti-C1q como Marcador de Nefritis Lúpica / Anti-C1q as Lupus Nephritis Marker

Introducción: Los autoanticuerpos anti-C1q han sido propuestos como un marcador útil en el lupus eritematoso sistémico por su asociación con la nefritis lúpica. Objetivo: Determinar la prevalencia de anti-C1q en pacientes con lupus eritematoso sistémico y otras enfermedades reumáticas para la evaluar la asociación con la nefropatía lúpica. Métodos: Se incluyeron 179 pacientes con lupus eritematoso sistémico y 82 con otras enfermedades reumáticas. La nefritis lúpica fue diagnosticada en 70 (39 por ciento) de los pacientes con lupus eritematoso sistémico. Los anticuerpos anti-C1q IgG se determinaron por ELISA. Las asociaciones se evaluaron por análisis de regresión logística. Resultados: La prevalencia de anti-C1q fue de 37 poe ciento (66/179) en los pacientes con lupus eritematoso sistémico y de 9 por ciento (7/82) en controles (OR = 6,3; IC 95 por ciento 2,8-14,1; p < 0,001). El anti-C1q fue asociado con proteinuria (OR = 2,6; IC 95 por ciento 1,2-6,0; p < 0,022); eritrosedimentación elevada (OR = 3,2; IC 95 por ciento 1,5-6,7; p < 0,003) y anti-DNAdc (OR = 3,9; IC 95 por ciento 1,7-9,1; p < 0,002). En el modelo de regresión logística ajustado para demografía y anti-DNAdc, aunque la OR del anti-C1q para la nefritis fue 2 veces más alta que en ausencia del anti-C1q, solo se aproximó a la significación estadística. La positividad simultánea de anti-C1q y anti-DNAdc estuvo asociada a la nefritis lúpica (OR = 4,3; IC 95 por ciento 1,9-9,5; p < 0,001). Conclusiones: El anti-C1q se presentó con mayor frecuencia en pacientes con lupus eritematoso sistémico que en los controles. El anti-C1q combinado con anti-DNAdc resultó fuertemente asociado a la nefritis lúpica(AU)

Introducción: Anti-C1q autoantibodies have been proposed as useful marker in systemic lupus erythematosus due to their association with lupus nephritis. Objective: To determine the prevalence of anti-C1q in patients with systemic lupus erythematosus and other rheumatic diseases to evaluate the association with lupus nephropathy. Methods: One hundred seventy-nine patients with systemic lupus erythematosus and 82 with other rheumatic diseases were included. Lupus nephritis was diagnosed in 70 (39percent) of patients with systemic lupus erythematosus. Anti-C1q IgG antibodies were determined by ELISA. Associations were evaluated by logistic regression analysis. Results: The prevalence of anti-C1q was 37percent (66/179) in patients with systemic lupus erythematosus and 9percent (7/82) in controls (OR = 6.3; 95percent CI 2.8-14). .1; p < 0.001). Anti-C1q was associated with proteinuria (OR = 2.6; 95percent CI 1.2-6.0; p < 0.022); elevated erythrocyte sedimentation rate (OR = 3.2; 95percent CI 1.5-6.7; p < 0.003) and anti-dsDNA (OR = 3.9; 95percent CI 1.7-9.1; p < 0.002). In the logistic regression model adjusted for demographics and anti-dsDNA, although the OR of anti-C1q for nephritis was 2-fold higher than in the absence of anti-C1q, it only approached statistical significance. Simultaneous positivity of anti-C1q and anti-dsDNA was associated with lupus nephritis (OR = 4.3; 95percent CI 1.9-9.5; p < 0.001). Conclusions: Anti-C1q occurred more frequently in patients with systemic lupus erythematosus than in controls. Anti-C1q combined with anti-dsDNA was strongly associated with lupus nephritis(AU)

In vivo evaluation of Clostridioides difficile enoyl-ACP reductase II (FabK) Inhibition by phenylimidazole unveils a promising narrow-spectrum antimicrobial strategy.

Clostridioides difficile infection (CDI) is a leading cause of hospital-acquired diarrhea, which often stem from disruption of the gut microbiota by broad-spectrum antibiotics. The increasing prevalence of antibiotic-resistant C. difficile strains, combined with disappointing clinical trials results for recent antibiotic candidates, underscore the urgent need for novel CDI antibiotics. To this end, we investigated C. difficile enoyl ACP reductase (CdFabK), a crucial enzyme in de novo fatty acid synthesis, as a drug target for microbiome-sparing antibiotics. To test this concept, we evaluated the efficacy and in vivo spectrum of activity of the phenylimidazole analog 296, which is validated to inhibit intracellular CdFabK. Against major CDI-associated ribotypes 296 had an MIC90 of 2 µg/ml, which was comparable to vancomycin (1 µg/ml), a standard of care antibiotic. In addition, 296 achieved high colonic concentrations and displayed dosed-dependent efficacy in mice with colitis CDI. Mice that were given 296 retained colonization resistance to C. difficile and had microbiomes that resembled the untreated mice. Conversely, both vancomycin and fidaxomicin induced significant changes to mice microbiomes, in a manner consistent with prior reports. CdFabK therefore represents a potential target for microbiome-sparing CDI antibiotics, with phenylimidazoles providing a good chemical starting point for designing such agents.

[Identification of Complex and Combined Antibody Consisted of Anti-c, Anti-E, Anti-Jka and Anti-Fya].

OBJECTIVE: To investigate the role of multiple serological methods in the identification of complex antibodies. METHODS: The blood group antigens were detected by saline and microcolumn agglutination methods. The saline method was used to screen and identify IgM-type antibodies in the patient's serum, while the polybrene, anti-globulin, microcolumn agglutination, enzymic and absorption-elution methods were used to screen and identify IgG-type antibodies. RESULTS: The patient was B/CCDee/Jk(a-b+)/Fy(a-b+) blood type. The serum reacted with panel cells, and the reaction presented anti-E pattern in the saline medium. It was fully positive in the microcolumn agglutination card, except 2 negative ones after using papain to treat the panel cells. Referring to the pattern table, it was concluded that there existed anti-c, anti-E, and anti-Jka antibodies, and one antibody corresponding to an antigen that was easily destroyed by papain. The red blood cells with specific phenotype were selected for absorption-elution to identify IgG-type anti-c, anti-E, anti-Jka and anti-Fya antibodies. CONCLUSION: It is confirmed that IgM-type anti-E, and IgG-type anti-c, anti-E, anti-Jka and anti-Fya antibodies exist in the patient's serum by multiple serological methods.

Detection of red cell alloantibody prior to overflow phenomenon in a case of warm AIHA secondary to Chronic Lymphocytic Leukemia and Myasthenia Gravis: A case report.

INTRODUCTION: Defects in the lymphoid system have been linked to immune dysregulation, which might explain why lymphoid neoplasms and immunological disorders tend to occur concurrently. Chronic Lymphocytic Leukemia (CLL), characterised by the accumulation of dysfunctional lymphocytes, is associated with autoimmune cytopenias such as autoimmune haemolytic anaemia (AIHA). Detection of underlying alloantibody in warm AIHA, is challenging for any transfusion medicine specialist. This report highlights the significance of overflow phenomenon in detection of alloantibody in a case of warm AIHA secondary to CLL and myasthenia gravis. CASE REPORT: A 56-year-old male with a history of myasthenia gravis and thymoma progressed to B-cell CLL presented with severe anaemia and thrombocytopenia leading to multiple red blood cell (RBC) transfusions in the last two months. Clinical profile and laboratory workup suggested features of AIHA, and subsequent immunohaematological workup hinted towards an impending overflow phenomenon due to differential reactivity pattern observed between serum and eluate with antibody screen/identification panel. The eluate was pan-reactive with an antibody screen/ identification panel, while the serum showed a discrete anti-C alloantibody pattern. A compatible and antigen-negative RBC unit was successfully transfused, followed by medical management. DISCUSSION: The overflow phenomenon in AIHA depends on antibody titre and its affinity for RBC antigens. In the index case, the impending 'overflow or spillover' of autoantibodies into the patient's serum allowed us to detect underlying alloantibody without performing allogeneic adsorption and transfuse antigen-negative and crossmatch compatible PRBC unit. CONCLUSION: This case emphasises the significance of understanding the overflow phenomenon in AIHA as it can guide a transfusion medicine specialist in the early detection and identification of underlying alloantibodies, which is crucial for appropriate transfusion management in AIHA. However, early presentation and timely workup, along with a high level of suspicion, is crucial to identify this phenomenon.

Acquired Non-histaminergic Angioedema With C1q Autoantibody and Urticaria: A Case Report.

Acquired angioedema (AAE) is a rare disease with life-threatening complications. This pathology has classically been associated with medication use and B cell lymphoproliferative disorders. In this report, we describe a 61-year-old man with a six-year history of angioedema, unrelated to any known triggers or malignancy. Extensive workup has led to a diagnosis of idiopathic nonhistaminergic AAE with normal C1 inhibitor. The patient is currently being treated with lanadelumab, which has resolved the patient's symptoms. This case provides insight into the onset, exploration, treatment, and outcomes of an extremely rare disease process.

Intestinal Colonization of Campylobacter jejuni and Its Hepatic Dissemination Are Associated with Local and Systemic Immune Responses in Broiler Chickens.

Campylobacter jejuni is an important foodborne pathogen. Despite the lack of clinical signs associated with its colonization in poultry, it has been reported to interact with the intestinal immune system. However, little is known about the interaction between C. jejuni and the chicken immune system, especially in the context of hepatic dissemination. Therefore, to follow up on our previous study showing intestinal colonization and hepatic spread of C. jejuni, cecal tonsils and liver samples were collected from these birds to determine the mRNA levels of chemokines and cytokines. Serum samples were also collected to determine serum amyloid A (SAA) concentrations and specific IgY titers. Lack of Th17 induction was observed in the cecal tonsils of only the liver-contaminated groups. This hepatic dissemination was accompanied by innate, Th1 and Th2 immune responses in livers, as well as an increase in SAA concentrations and specific IgY levels in sera. Campylobacter appears to be able to restrain the induction of the chicken gut immunity in particular conditions, possibly enhancing its hepatic dissemination and thus eliciting systemic immune responses. Although Campylobacter is often recognized as a commensal-like bacterium in chickens, it seems to modulate the gut immune system and induce systemic immunity.

Combination of anti-C1qA08 and anti-mCRP a.a.35-47 antibodies is associated with renal prognosis of patients with lupus nephritis.

Objective: The aim of this study is to explore the prevalence and clinicopathological associations between anti-C1qA08 antibodies and anti-monomeric CRP (mCRP) a.a.35-47 antibodies and to explore the interaction between C1q and mCRP. Methods: Ninety patients with biopsy-proven lupus nephritis were included from a Chinese cohort. Plasma samples collected on the day of renal biopsy were tested for anti-C1qA08 antibodies and anti-mCRP a.a.35-47 antibodies. The associations between these two autoantibodies and clinicopathologic features and long-term prognosis were analyzed. The interaction between C1q and mCRP was further investigated by ELISA, and the key linear epitopes of the combination of cholesterol binding sequence (CBS; a.a.35-47) and C1qA08 were tested by competitive inhibition assays. The surface plasmon resonance (SPR) was used to further verify the results. Results: The prevalence of anti-C1qA08 antibodies and anti-mCRP a.a.35-47 antibodies were 50/90 (61.1%) and 45/90 (50.0%), respectively. Levels of anti-C1qA08 antibodies and anti-mCRP a.a.35-47 antibodies were negatively correlated with serum C3 concentrations ((0.5(0.22-1.19) g/L vs. 0.39(0.15-1.38) g/L, P=0.002) and (0.48(0.44-0.88) g/L vs. 0.41(0.15-1.38) g/L, P=0.028), respectively. Levels of anti-C1qA08 antibodies were correlated with the score of fibrous crescents and tubular atrophy (r=-0.256, P=0.014 and r=-0.25, P=0.016, respectively). The patients with double positive antibodies showed worse renal prognosis than that of the double negative group (HR 0.899 (95% CI: 0.739-1.059), P=0.0336). The binding of mCRP to C1q was confirmed by ELISA. The key linear epitopes of the combination were a.a.35-47 and C1qA08, which were confirmed by competitive inhibition experiments and SPR. Conclusion: The combination of anti-C1qA08 and anti-mCRP a.a.35-47 autoantibodies could predict a poor renal outcome. The key linear epitopes of the combination of C1q and mCRP were C1qA08 and a.a.35-47. A08 was an important epitope for the classical pathway complement activation and a.a.35-47 could inhibit this process.

Anti-C causing severe hemolytic disease of the fetus and newborn: a rare case report.

Hemolytic disease of the fetus and newborn (HDFN) due to anti-D was severe and fatal before the development of RhD immune prophylaxis. Proper screening and universal administration of Rh immune globulin has decreased the incidence of HDFN to a great extent. Pregnancy, transfusion, and transplantation still increase the chances of other alloantibody formation and the potential for HDFN. Advanced methods for immunohematology investigation allow for the identification of alloantibodies causative for HDFN other than anti-D. Many antibodies have been reported to cause HDFN, but there is scant literature where isolated anti-C is responsible for HDFN. We present here a case of severe HDFN caused by anti-C leading to severe hydrops and death of the neonate despite three intrauterine transfusions and other measures.

Comparison of outcomes after plasma therapy or eculizumab in pediatric patients with atypical hemolytic uremic syndrome.

BACKGROUND: Atypical hemolytic uremic syndrome (aHUS) is an ultra-rare and life-threatening disease. For decades, plasma therapy was used to manage patients with aHUS. Since eculizumab, a recombinant humanized anti-C5 monoclonal antibody, was approved for treatment of aHUS, it has been used to treat patients with aHUS. Here, we examined the effectiveness of eculizumab and plasma therapy, respectively in the treatment of pediatric patients with aHUS. METHODS: Data were collected from questionnaires sent to 75 institutions known to be treating thrombotic microangiopathy (TMA). RESULTS: A total of 24 patients were evaluable, in which no recurrence of TMA was reported at last observation. There were four therapy groups: two patients receiving supportive therapy, one receiving plasma therapy alone, 17 switching from plasma therapy to eculizumab (therapy switched), and four receiving eculizumab alone. Among 17 patients of therapy-switched group, only one patient achieved complete remission at the end of plasma therapy, 15 patients achieved complete remission after eculizumab initiation, and two patients reached end-stage renal disease. Adverse events were reported in nine cases; among these, meningococcal infection, anaphylaxis, and eculizumab-related infusion reaction were reported among those treated with eculizumab. CONCLUSION: This study provided substantial evidence from a Japanese population that the conversion from plasma therapy to eculizumab therapy should be considered in patients with aHUS who show an incomplete response to plasma therapy. In addition, although no new safety events were detected, careful attention should be paid to meningococcal infection, eculizumab-related infusion reactions and allergic reactions with administration of eculizumab.

Correlation between anti-C1q antibody and disease activity and cellular immune function in patients with systemic lupus erythematosus / 中国医师杂志

Objective:To evaluate the correlation between anti-C1q antibody and disease activity and cellular immune function in patients with systemic lupus erythematosus (SLE).Methods:The clinical data and test indexes of 134 patients with SLE and 90 healthy people who were admitted to Henan Provincial People′s Hospital from June 2017 to February 2018 were collected. The level of anti-C1q antibody was measured by enzyme-linked immunosorbent assay (ELISA), and lymphocyte subsets were measured by flow cytometry. According to the score of Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)-2K, SLE patients were divided into active and inactive groups, and SLE patients were divided into LN group and non-LN group according to the presence or absence of kidney involvement. The levels of anti-C1q antibodies and lymphocyte subsets were compared among the three groups, and correlations between anti-C1q antibodies and disease activity and lymphocytes were analyzed. The predictive value of anti-C1q antibodies and anti double stranded DNA (dsDNA) antibodies for SLE disease activity was evaluated.Results:The anti-C1q antibody level, percentage of T cells and Ts cells in SLE group were higher than those in control group, while the percentage of Th cells, percentage of NK cells, T cell count, Th cell count, B cell count and NK cell count in SLE group were lower than those in control group (all P<0.05); The anti-C1q antibody level in the active group was higher than that in the inactive group, and the counts of T cells, Ts cells, Th cells, B cells and NK cells were lower than those in the inactive group (all P<0.05); The anti-C1q antibody level in LN group was higher than that in non-LN group, and the T cell count, Ts cell count, Th cell count, B cell count, NK cell count were lower than that in non-LN group, with statistically significant difference (all P<0.05). Correlation analysis showed that age, hemoglobin (HB), C3, C4, T cell count, Th cell count, B cell count and NK cell count were negatively correlated with anti-C1q antibody, while SLEDAI-2K, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and anti-dsDNA antibody were positively correlated with anti-C1q antibody (all P<0.05). Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) of anti-C1q antibody alone in predicting SLE disease activity was 0.702, with a sensitivity of 0.547 and a specificity of 0.827. The combination of anti-C1q and anti ds-DNA antibodies resulted in an AUC of 0.761, a sensitivity of 0.756, and a specificity of 0.691. The combined detection value of the two antibodies predicting SLE disease activity was better than the single detection. Conclusions:Anti-C1q antibody is closely related to disease activity and cellular immune dysfunction, and has certain predictive value in SLE disease activity.

Identification of immune hemolytic transfusion reaction and exploration of transfusion compatibility testing / 中国输血杂志

【Objective】 To analyze the causes of immune hemolytic transfusion reaction in one case, identify related antibodies, and explore transfusion compatibility testing. 【Methods】 ABO/Rh blood group identification, unexpected antibody identification of serum and diffusion fluid, direct antiglobulin test(DAT) and cross matching were conducted by saline method and/or microcolumn gel method. 【Results】 The patient′s blood group was O, and Rh phenotype was identified as DCCee. The DAT was negative, with strong anti-E antibody and weak anti-c antibody detected. Acute hemolytic transfusion reaction occurred in the patient after the last transfusion. 【Conclusion】 Currently, immune hemolytic transfusion reaction in China are mainly caused by Rh blood group system antibodies. The absence of unexpected antibody screening before blood transfusion and the weak anti-c antibody which resulted in missed detection of non compatibility in cross matching led to acute hemolytic transfusion reaction. It is recommended to conduct unexpected antibody screening before blood transfusion, and to collect blood sample for testing as soon as possible to improve the accuracy of DAT when acute hemolytic transfusion reaction is suspected.

Identification of Complex and Combined Antibody Consisted of Anti-c, Anti-E, Anti-Jka and Anti-Fya / 中国实验血液学杂志

OBJECTIVE@#To investigate the role of multiple serological methods in the identification of complex antibodies.@*METHODS@#The blood group antigens were detected by saline and microcolumn agglutination methods. The saline method was used to screen and identify IgM-type antibodies in the patient's serum, while the polybrene, anti-globulin, microcolumn agglutination, enzymic and absorption-elution methods were used to screen and identify IgG-type antibodies.@*RESULTS@#The patient was B/CCDee/Jk(a-b+)/Fy(a-b+) blood type. The serum reacted with panel cells, and the reaction presented anti-E pattern in the saline medium. It was fully positive in the microcolumn agglutination card, except 2 negative ones after using papain to treat the panel cells. Referring to the pattern table, it was concluded that there existed anti-c, anti-E, and anti-Jka antibodies, and one antibody corresponding to an antigen that was easily destroyed by papain. The red blood cells with specific phenotype were selected for absorption-elution to identify IgG-type anti-c, anti-E, anti-Jka and anti-Fya antibodies.@*CONCLUSION@#It is confirmed that IgM-type anti-E, and IgG-type anti-c, anti-E, anti-Jka and anti-Fya antibodies exist in the patient's serum by multiple serological methods.