Mandibular Osteomyelitis in Concurrence with Psoriasis: A Rare Case Report and Literature Review

Mandibular osteomyelitis in a patient with psoriasis is an uncommonly clinical manifestation while there is an increasing number of reports and studies on involvements of stomatology in psoriasis, especially the death of a patient via or not via Allogeneicbone marrow transplantation has never been reported.To review the management and possible mechanisms in pathogenesis and treatment of psoriasis, as well as the relative involvements between stomatology and psoriasis the typical case with pictures and files is reviewed and literature is collected.Wekeepthe knowledge that psoriasis is either a primary keratinocyte disorder or an immunocyte-mediated chronic skin inflammatorydisease while bone marrow is under suspected for immunopathogenesis. More association of stomatologic conditions with psoriasis is emerging. Conclusively, allogeneicBMT and new knowledge are worth to be stressed by both stomatological and dermatological doctors. Further insights of this kind of auto immunologic disease are under its developing.

Aspectos clínicos e inmunopatogénicos de la alopecia areata / Clinical and immunopathogenical aspects of alopecia areata

Resumen La alopecia areata en una enfermedad autoinmune caracterizada por pérdida no cicatricial de pelo, en forma de parches localizados o generalizados, en la que se pierde el privilegio inmunológico del folículo piloso. Factores ambientales, neuroendocrinos y/o psicológicos en individuos genéticamente predispuestos llevan a la activación inmunológica que conduce a la alopecia. La tercera parte de los pacientes tienen familiares afectados y se ha descrito asociación con antígenos del HLA clase I y II, y de polimorfismos de nucleótido único en genes relacionados con la activación del linfocito T. Neuropéptidos como la sustancia P, el péptido relacionado con el gen de la calcitoninay el péptido intestinal vasoactivo, producidos por los nervios cutáneos, participan en la inmunopatogénesis. Como otras entidades dermatológicas, puede ser subestimada y catalogada como un problema estético, sin tener en cuenta que tiene alto impacto en la calidad de vida y se asocia a comorbilidades psiquiátricas, autoinmunes y endocrinas.

Summary Alopecia areata (AA) is an autoimmune disease characterized by non-cicatricial hair loss, in the form of localized or generalized patches, in which the immunological privilege of the hair follicle is lost. Environmental, neuroendocrine and / or psychological factors in genetically predisposed individuals lead to immune activation and hence, alopecia. One third of the patients has affected relatives, association with HLA class I and II antigens, and single nucleotide polymorphisms in genes related to the activation of the T lymphocyte. Neuropeptides such as substance P, the peptide related to the Calcitonin gene and vasoactive intestinal peptide, produced by cutaneous nerves, participate in the immunopathogenesis of AA. Like other dermatological entities, it can be underestimated and cataloged as an aesthetic problem, without considering its high impact on quality of life and its association with psychiatric, autoimmune and endocrine comorbidities.

Interpretation of the pathogenesis part of Clinical Practice Guideline:Diagnosis and Treatment in Children with Allergic Rhinitis / 中国实用儿科杂志

Allergic rhinitis(AR)in children is non-infectious chronic inflammatory disease in the nasal mucosa which was largely determined by IgE when the body is exposed to allergens. It was believed that Th1/Th2 immune imbalance is the main pathogenesis of AR;however,more and more studies put emphasis on the integrality of individual immune system of the disease. Systematic discussion on the pathogenesis of natural immunity and acquired immunity in allergic rhinitis may provide useful AR treatments in the future.

COMPARISON OF PATHOGENESIS OF P. BERGHEIINFECTION IN MOUSE AND RAT MODELS

@#Background: The cytokine cascade in the immunopathogenesis of malaria infection had been widely studied. However, their specific association with survival and severe infection remained obscure.Methods: Thestudy investigated the cytokine profiles and histopathological features of malaria in the severe infection and survival models by using male ICR mice and male Sprague Dawley rats respectively.Results: The severe model, the infected ICR mice, exhibited a high parasitemia with 100% mortality after peak parasitemia at day 5 post-infection. The survival model, the infected Sprague Dawley rats, showed mild parasitemia with full recovery by day 14 of infection. Both severe and survival models showed similar histopathological severity during peak parasitemia. The severe model produced highly elevated levels of pro-inflammatory cytokines, TNF-α and IL-1α, and low levels of the anti-inflammatory cytokine, IL-4; while the survival model showed low levels of TNF-α and IL-1α with high levels of IL-4.Conclusion: There were differences in the pathogenesis of the severe and survival models of malaria infection. These could be a basis for immunotherapy of malaria in the future

Upregulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in renal tissue in severe dengue in humans: Effects on endothelial activation/dysfunction

Abstract INTRODUCTION: Dengue is an important mosquito-borne disease in tropical and subtropical regions. Adhesion molecules have not been systematically characterized in the renal tissue of patients with severe dengue (SD). The objective of this study was to detect viral antigens in samples from patients that evolved with SD, correlating with the expression of ICAM-1, VCAM-1, VE-cadherin, and E-selectin to contribute to a better understanding of the pathophysiology of SD. METHODS: Kidney specimens from patients with SD were selected according to clinical and laboratorial data and submitted to histological and immunohistochemistry analysis. A semiquantitative evaluation was performed considering positive immunostaining in 20 glomeruli. RESULTS: Viral antigens were mainly detected in distal tubules. The intense immunostaining of VCAM-1 and ICAM-1 was observed. The expression of E-selectin was discrete, and VE-cadherin expression varied from mild to moderate. VCAM-1 was slightly intense in the glomerular capsule; the expression of ICAM-1 was diffuse. E-selectin was diffuse, and VE-cadherin varied from mild to moderate. The most frequent histological findings were glomerular congestion, mild glomerulitis, acute renal injury, and glomerular atrophy. CONCLUSIONS: The results appear to demonstrate an imbalance between vascular endothelial permeability regulating events in renal lesions in SD. The increase in the expression of ICAM-1 and VCAM-1 is an in-situ indicator of higher permeability with a consequent influx of cells favoring the inflammation of the endothelium. These molecules are important in the pathophysiology of the disease and provide the possibility of developing new markers for the evaluation, clinical follow-up, and therapeutic response of patients with SD.

Inmunopatogenia de la psoriasis: nuevos avances / Inmunopatogenia of psoriasis. New progress

La psoriasis es una enfermedad inflamatoria crónica de la piel. Su etiología es multifactorial e incluye susceptibilidad genética, factores inmunológicos y múltiples elementos ambientales, que pueden desencadenar y/o exacerbar la enfermedad. En las últimas décadas se han realizado investigaciones minuciosas sobre la patogénesis de la psoriasis, han sido reconocidos varios subtipos de células T que tienen un papel fundamental en el establecimiento de la inflamación en lesiones cutáneas. Los estudios genéticos brindan las bases para la construcción del modelo de la enfermedad, demostrando que las células dendríticas, los linfocitos T y los queratinocitos desempeñan un rol clave en la patología de esta entidad, así como también un conjunto de citoquinas que impulsan la inflamación psoriásica, dentro de las que se incluyen TNFα, IL-22, IL-23 e IL-17, las cuales promueven la respuesta inflamatoria de queratinocitos, y la producción de péptidos antimicrobianos, citoquinas y quimiocinas, perpetuando así la respuesta inflamatoria. En la actualidad, el desarrollo de varios fármacos biológicos altamente eficaces ha revolucionado el tratamiento de la psoriasis en placas de moderada a severa. Estos medicamentos son un reflejo de una mayor comprensión de la patogénesis de la psoriasis, incluyendo la importancia central de IL-23 e IL17 y las diferentes vías de señalización. El objetivo de este trabajo es realizar una revisión crítica de la literatura sobre la psoriasis y los mecanismos implicados en su imnunopatogenia(AU)

Psoriasis is a chronic inflammatory disease of the skin. Its etiology involves several agents such as genetic susceptibility, immunological factors and multiple environmental elements, which can trigger and / or exacerbate the disease. In recent decades thorough research has been conducted on the pathogenesis of psoriasis, several T-cell subtypes that play a key role in the establishment of inflammation in skin lesions have been recognized. Genetic studies provide the basis for the construction of the disease model, demonstrating that dendritic cells, T lymphocytes and keratinocytes play a key role in the pathology of this entity, as well as a set of cytokines that drive psoriatic inflammation , such as include TNF , IL-22, IL-23 and IL-17, which promote the inflammatory response of keratinocytes, and the production of antimicrobial peptides, cytokines and chemokines, thus perpetuating the inflammatory response. At present, the development of several highly effective biological drugs has revolutionized the treatment of moderate to severe plaque psoriasis. These drugs are a reflection of a greater understanding of the pathogenesis of psoriasis, including the central importance of IL-23 and IL-17 and different signaling pathways. The objective of this work is to perform a critical review of the literature on psoriasis and the mechanisms involved in its imnunopathogenesi(AU)

n-3 polyunsaturated fatty acids supplementation in psoriasis: a review

Psoriasis is an immune mediated chronic inflammatory disease of unknown etiology and characterized by epidermal hyperplasia and inappropriate immune activation, which affects the skin and joints as well.The immunopathogenesis of psoriasis involves changes in the innate and acquired (T lymphocytes) immune system. The cells of the innate immune system when activated produce growth factors, cytokines, and chemokines that act on cells of the acquired immune system and vice versa, being characterized as atype 1 immune response disease. Fish oil n-3 polyunsaturated fatty acids, mainly eicosapentaenoic (EPA), and docosahexaenoic acids (DHA), reduce symptoms in many inflammatory skin diseases. The mechanism of action of fish oil in the treatment of psoriasis is widely based on the alteration of epidermal and blood cell membrane lipid composition. In the present study, we performed a review of the several studies, which analyzed the action of n-3 polyunsaturated fatty acids in patients with psoriasis. Taken together, the majority of the studies showed that n-3 polyunsaturated fatty acids, mainly from marine origin, have beneficial effects and can be utilized as adjuvant therapy in psoriasis treatment. Both oral and intravenous administration of fish oil n-3 polyunsaturated fatty acids had positive effects. However, further studies are warranted to answer many intriguing questions, for instance, the ideal quantity of fish oil to be utilized, the effect on different forms and severity of psoriasis and last, but not least, the consequences of using fish oil n-3 polyunsaturated fatty acids on the cardiovascular features of patients with psoriasis.

Papel de las células dendríticas en la infección por el virus dengue: blancos de replicación y respuesta inmune / Role of dendritic cells in infection by dengue virus: targets for replication and immune response

Dengue fever, caused by dengue virus (DENV) infection, is one of the most important diseases in the world, not only due to the high morbidity/mortality rates it causes, but also because of its great economic and social impact in tropical/subtropical countries. DENV infection has a wide range of clinical manifestations ranging from asymptomatic infection or infection with mild symptoms to severe dengue that can lead to death. At present, no etiological treatment or effective globally distributed vaccine against the four DENV serotypes exists. Despite great efforts made to understand the mechanism associated with DENV disease pathogenesis the causes leading to severe dengue presentation have not been clarified. Some hypotheses seek to give a biological and physiological explanation to the clinical manifestations that appear during the infection. Based on the evidence that after contact with dendritic cells DENV alters the functionality of these cells, this review aims to describe the most relevant findings regarding the importance of dendritic cells in the context of DENV infection and progression of the illness.

El dengue, causada por el virus dengue (DENV), es una de las enfermedades más importantes no sólo por los altos índices de morbilidad/mortalidad, sino también por su gran impacto económico y social en los países de las regiones tropicales/subtropicales. La infección por el DENV cursa por un variado rango de manifestaciones clínicas que van desde una infección asintomática o con síntomas leves, hasta el dengue grave que puede ser fatal. En la actualidad, no se dispone de un tratamiento etiológico y tampoco de una vacuna eficaz mundialmente distribuida, contra los 4 serotipos del DENV. A pesar de los grandes esfuerzos orientados a entender el mecanismo asociado con la patogénesis de la enfermedad, aún no se ha logrado esclarecer de forma definitiva las causas que conllevan a las formas graves de enfermedad. Algunas hipótesis buscan dar una explicación biológica y fisiológica a las manifestaciones clínicas que se presentan durante la infección. Dado que una de ellas sugiere que luego del contacto con las células dendríticas el DENV altera su funcionalidad, la presente revisión tiene como objetivo describir los hallazgos más relevantes referentes a la importancia de dichas células en el marco de la infección por el DENV y progresión de la enfermedad.

Functions of NK cells in chronic hepatitis B patients treated with interferon / 中华实验和临床病毒学杂志

Objective@#To elucidate the functions of peripheral blood NK cells in chronic hepatitis B patients treated with interferon.@*Methods@#Venous whole blood samples were obtained from patients in the immune clearance (IC) phase treated with peg-interferon-alpha-2a (Peg-IFNα-2a) at baseline (t=0), 12 weeks (t=12) and 24 weeks (t=24). The frequencyies of peripheral blood CD3-CD56+ NK cells, CD56brightNK cells and CD56dimNK cells, the expression level of IFNAR2 and NKp46 on NK cells were detected by flow cytometry. The levels of serum HBV DNA, HBsAg, HBeAg and ALT were detected by Ditan Hospital clinical laboratory.@*Results@#Forty-one patients in the IC phase treated with Peg-IFNα-2a, including 21 poor response (PR) patients and 20 good response (GR) patients, were recruited for this study. Theresult were as follows: The frequency of peripheral blood CD3-CD56+ NK cells was increased at week 24 in GR compared with the baseline(11.74, 5.69%-18.15% vs 13.7, 9.36-20.18%, P>0.05), and it also was increased in PR(8.94, 6.26%-14.15% vs 12.5, 7.64-16.55%, P>0.05). The frequency of peripheral blood CD56brightNK cells was increased at week 24 in GR compared with the baseline(9.49, 6.2%-12.48% vs 12.98, 7.75%-20.93%, P>0.05), and it also was increased in PR(11.45, 8.27%-19.13% vs 17.52, 12.3%-22.42%, P=0.0239). The expression level of NKp46 on NK cells was significantly increased at week 24 in GR compared with the baseline(90.55, 83.8-94.78 vs 93.8, 92.28-96.4, P=0.0263), but it was not increased in PR(95, 90.6-96.15 vs 94.3, 92.1-95.6, P>0.05). The expression level of NKp46high on NK cells was significantly increased at week 24 in GR compared with the baseline(12.4, 8.58-19.08 vs 39.3, 23.15-49.3, P=0.0011), at that range of the increase was significantly higher than PR(14.2, 9.78-17.65 vs 27.58, 19.13-36.56, P=0.006).@*Conclusions@#The frequencies of peripheral blood CD3-CD56+ NK cells and CD56brightNK cells were increased from patients in the IC phase treated with Peg-IFNα-2a. The expression level of NKp46 on NK cells was increased in GR patients treated with Peg-IFNα-2a. The expression level of NKp46high on NK cells was significantly increased, especially in GR patients treated with Peg-IFNα-2a.

Research progress in pathogenesis of herpes simplex keratitis / 中华实验眼科杂志

Herpes simplex keratitis (HSK) is a global high incidence of serious infectious cause of blindness.Chronic visual impairment and visual loss are caused by recurrence of infection,corneal scaring,keratoleukoma,corneal vascularization,lymphangion and so on.According to the current study,corneal injury is the result of chronic inflammatory reaction against herpes simplex virus (HSV) antigens.Because of its unclear pathogenesis,the treatment methods do not get satisfactory results.Overall understanding of first infection,latent and recurrent mechanism of the disease is the precondition for its effective treatment.By describing the role of autophagy,immune system,cytokines and miRNAs in the mechanism of HSK infection and pathogenesis,the readers can understand the process of the occurrence and development in HSK,to some degree,it will not only provide some references for the diagnosis of HSK,but also bring some new inspirtion in treatment and drug development.

CD4+CD25+FoxP3+Treg in the immune mechanism of severe mycoplasma pneumoniae pneumonia in children / 国际儿科学杂志

Objective To investigate the role of CD4+CD25+FoxP3+ in severe Mycoplasma pneumonia among children.Methods One hundred and forty children with M.pneumoniae pneumonia (65 severe and 75 non-severe) who were hospitalized were enrolled along with forty other children as controls.X-ray was assessed.The proportions of peripheral blood CD4+CD25+FoxP3+cells were determined by flow cytometry.Results Both severe and non-severe children had decreased CD4+CD25+FoxP3+cells as compared with control subjects in acute phase (0.87 ± 0.66％ vs.3.88 ± 2.00％,P ＜ 0.01 and 1.17 ± 0.70％ vs.3.88 ±2.00％,P ＜0.01,respectively).The levels of CD4+CD25+FoxP3+cells in severe children were lower than those in non-severe children in acute phase and recovery phase (0.87 ±0.66％ vs.1.17 ±0.70％,P ＜0.05 and 1.66 ±0.85％ vs.3.61 ± 1.45％,P＜0.01,respectively).Both severe children and non-severe children expressed higher CD4+CD25+FoxP3+cells in recovery phase than in acute phase (1.66 ± 0.85 ％ vs.0.87 ± 0.66％,P ＜0.01 and 3.61 ± 1.45％ vs.1.17 ±0.70％,P ＜0.01,respectively).Conclusion The expression of CD4+CD25+FoxP3+Tregs may play a role in the onset of severity of mycoplasma pneumonia and the low express of CD4+CD25+FoxP3+Tregs in children infected with M.pneumonia may increase the susceptibility to severe mycoplasma pneumonia.

Progress in the study of hematopoietic stem cell transplantation in the treatment of psoriasis / 中国综合临床

Objective Hemapoietic stem cell (HSC) is a kind of pluripotent cell which can differentiate into different kinds of cells,including blood cells and immune cells.Hemapoietic stem cell transplantation(HSCT) is to destory abnormal bone marrow hematopoietic cells,and imbed healthy stem cells to reconstruct hematopoiesis and immune system,and it is an effective therapy for the treatment of hematopoietic malignances,genetic and metabolic disease,autoimmune disease and solid tumor.At present,it has been widely used to treat the patients with hematologial malignant tumors,such as lymphoma and leukemia.Clinical investigation showed that patients with leukemia and psoriasis after HSCT,both leukemia and psoriasis were cured.In this review,the immunopathogenesis of psoriasis,the possible mechanism of psoriasis associated with leukemia,the immunopathogenesis of HSCT and the theory basis of treating psoriasis and the application of HSCT in the treatment of psoriasis with leukemia were comprehensively discussed.

A Common Immunopathogenesis Mechanism for Infectious Diseases: The Protein-Homeostasis-System Hypothesis / 감염과화학요법

It was once believed that host cell injury in various infectious diseases is caused solely by pathogens themselves; however, it is now known that host immune reactions to the substances from the infectious agents and/or from the injured host cells by infectious insults are also involved. All biological phenomena in living organisms, including biochemical, physiological and pathological processes, are performed by the proteins that have various sizes and shapes, which in turn are controlled by an interacting network within the living organisms. The author proposes that this network is controlled by the protein homeostasis system (PHS), and that the immune system is one part of the PHS of the host. Each immune cell in the host may recognize and respond to substances, including pathogenic proteins (PPs) that are toxic to target cells of the host, in ways that depend on the size and property of the PPs. Every infectious disease has its own set of toxic substances, including PPs, associated with disease onset, and the PPs and the corresponding immune cells may be responsible for the inflammatory processes that develop in those infectious diseases.

Immunopathogenesis and Treatment of Rheumatoid Arthritis: Recent Developments.

Rheumatoid arthritis (RA) is a chronic inflammatory disease occurring three times more in females throughout the world affecting 1-2% of the adult population in all ethnic groups, usually in the age group of 25-60 years. Although the role of CD4 + T helper lymphocytes in the aetiopathogenesis has been studied for more than three decades, the focus on CD4 + T helper type 17 (Th17) lymphocytes and its associated cytokines is much more recent. The cytokines such as IL-17 and IFN-g induce secondary cytokines such as IL-1, TNF-a , etc which possibly cause inflammation in joints. This cytokine cascade, therefore, offers a number of points and opportunities for immunointervention in RA. The present review article highlights some of the major aspects of the immunopathogenesis that involve Th17 cells and their association relevant to recent developments in the treatment of RA.

Dengue: an overview

Dengue is one of the highest occurring vector-borne diseases. It is caused by dengue viruses 1- 4. Currently, the disease is classified into dengue with or without warning signs and severe dengue based on WHO 2009 dengue classification. As of today, neither specific drugs nor commercial vaccine exist for dengue. The best treatment yet would be support, management and proper medical care. With no pathognomonic features that could differentiate it from other febrile illnesses, clinical diagnosis alone is insufficient. Yet, despite the current advances and existence of various laboratory diagnostic methods of dengue, a consensus singular method has not been established. There are several hypotheses or theories regarding the vaguely understood immunopathogenesis of dengue. Amongst these are the viral factors, host-immune factors and host-genetic factors. In addition to these, the occurrence of asymptomatic dengue has further complicated the disease. However, these individuals provide opportunities in the search for protective factors against dengue.

Role of Type I Interferon during Bacterial Infection

Type 1 Interferons (T1 IFN) play a pivotal role in innate immune responses against viral infection. Recently, this anti-viral cytokines are shown to be induced during bacterial infections via activation of various pattern recognition receptors (PRRs) including Toll-like receptors, RIG-I-like receptors, or NOD-like receptors. Signaling mediators such as MyD88, TRIF, MAVS, STING, or RIP2 of the receptor signaling pathways are also involved in T1 IFN responses depending on the bacterial species and their ligands. However, role of T1 IFN in anti-bacterial immunity is still obscure and its effect on immunological pathogenesis during bacterial infection has been controversial. It has been reported that T1 IFN could provide protective effect on several bacterial infections but it also aggravates pathogenic situation during some intracellular pathogens or secondary bacterial infection after respiratory viral infection. Here, we summarize recent findings how T1 IFN is induced by various bacterial pathogens and discuss the potential effect of T1 IFN responses on immune responses against bacterial infection.

Revisiting the Rich's formula: an update about granulomas in human tuberculosis

The formula proposed by Rich in 1951 explained the formation in a tuberculous lesion in a period that was unknown cellular functions, cytokines and other immunological aspects involved in granuloma formation by tuberculosis; its components are assembled conceptually to explain the pathogenic mechanisms involved in the granulomatous lesion in tuberculosis. In this manuscript, we report an update of Rich's formula based on the new and old concepts about pathogenic mechanisms involved in the granulomatous lesion in tuberculosis. Current knowledge allows us to conclude that the balance between the characteristics of the bacillus and host protective response is necessary to indicate the outcome of pathogenesis, infection or active disease and the necrosis degree of the tuberculosis lesion.

Immunopathogenesis of Allergic Asthma: More Than the Th2 Hypothesis

Asthma is a chronic obstructive airway disease that involves inflammation of the respiratory tract. Biological contaminants in indoor air can induce innate and adaptive immune responses and inflammation, resulting in asthma pathology. Epidemiologic surveys indicate that the prevalence of asthma is higher in developed countries than in developing countries. The prevalence of asthma in Korea has increased during the last several decades. This increase may be related to changes in housing styles, which result in increased levels of indoor biological contaminants, such as house dust mite-derived allergens and bacterial products such as endotoxin. Different types of inflammation are observed in those suffering from mild-to-moderate asthma compared to those experiencing severe asthma, involving markedly different patterns of inflammatory cells and mediators. As described in this review, these inflammatory profiles are largely determined by the involvement of different T helper cell subsets, which orchestrate the recruitment and activation of inflammatory cells. It is becoming clear that T helper cells other than Th2 cells are involved in the pathogenesis of asthma; specifically, both Th1 and Th17 cells are crucial for the development of neutrophilic inflammation in the airways, which is related to corticosteroid resistance. Development of therapeutics that suppress these immune and inflammatory cells may provide useful asthma treatments in the future.

Inmunopatogenia de la psoriasis. Impacto en las manifestaciones clínicas y el tratamiento de la enfermedad / Immunopathogenesis of psoriasis. Impact on clinical manifestations and its treatment

La psoriasis es una enfermedad inflamatoria crónica de la piel mediada por células T que afecta a individuos con predisposición genética y presenta varios subtipos clínicos. Se caracteriza por la presencia de placas eritematosas bien definidas, escamosas y de bordes irregulares, que afectan fundamentalmente las regiones de los codos, las rodillas, el cuero cabelludo y el tronco. El alelo HLA-Cw6 del sistema principal de histocompatibilidad está relacionado con la presencia y severidad de la enfermedad. Desde el punto de vista fisiopatogénico, la psoriasis es una enfermedad inmune de tipo Th1, en la que es fundamental el eje IL-23/Th17. Las células Th17 producen las citocinas proinflamatorias (IL-17A, IL-17F, IL-22 e IL-26) que activan los queratinocitos y causan hiperproliferación y mayor producción de citocinas proinflamatorias y péptidos antimicrobianos, los que a su vez reclutan y activan otras células inmunes de la piel inflamada. Se produce así una amplificación de la respuesta inflamatoria que conduce a las manifestaciones clínicas de la enfermedad. El tratamiento de la psoriasis incluye agentes antiinflamatorios tópicos, fototerapia, inmunosupresores sistémicos y agentes biológicos, entre los que se encuentran las proteínas de fusión, los inhibidores del factor de necrosis tumoral alfa y los inhibidores de las interleucinas 12 y 23

Psoriasis is a T cell-mediated chronic inflammatory disease of the skin. It affects genetically predisposed individuals and presents several subtypes. It is characterized by the presence of well-defined erythematous, scaly, irregular border plaque or lesions, affecting mainly the elbows, knees, scalp, and trunk. The HLA-Cw6 allele of major histocompatibility system is related to the presence and severity of this disease. From the physiopathogenic viewpoint, psoriasis is a Th1-type immune disease in which the axle IL-23/Th17 is fundamental. Th17 cells produce proinflammatory cytokines (IL-17A, IL-17F, IL-22 and IL-26) which activate keratinocytes and cause hyperproliferation and increased production of proinflammatory cytokines and antimicrobial peptides. The latter, in turn, recruit and activate other immune cells of swollen skin. There is thus an amplification of the inflammatory response that leads to clinical manifestations of this disease. The treatment of psoriasis includes topical antiinflammatory agents, phototherapy and systemic immunosuppressive biological agents, including those which are fusion proteins, inhibitors of alpha tumor factor necrosis, and interleukin inhibitors 12 and 23

Immunolooic mechanisms of severe mvcoplasma penumoniae Pneumonia in children / 国际儿科学杂志

Severe mycoplasma pneumoniae pneumonia is indicated as severe clinical symptoms,long course of disease,many extrapulmonary complications and the response to conventional therapy is poor.Its incidence has been increasing day by day,the inefficiency of host resistance to m ycoplasma pneumoniae,disorders of immune response and pathogenic immune escape are suggested to play critical roles in the immune mechanism of severe mycoplasma pneumoniae pneumonia.This paper summarizes the progress of immunopathogenesis of severe pneumoiae pneumonia in children.