Distribution of inflammatory cells in early atherosclerosis / 中国药理学通报

Aim To analyze the composition of immune cells in the inflammatory microenvironment of early atherosclerotic mice.Methods ApoE mice fed with high fat diet were userl to establish early athero¬sclerotic mouse model, and C57BL/6 mice fed normal diet were used as control.Oil red 0 staining, Masson's staining anrl biochemical analyzer were used to evaluate the success of the model construction.Infiltration of in¬nate immune cells and adaptive immune cells in aorta, peripheral blood, spleen and bone marrow of mice was detected and analyzed by flow cytometry.Results Compared with C57 mice, lipids infiltration in aortic root of ApoE mice increased and lipids level signifi¬cantly increased ( P < 0.01 ).Compared with those of C57 mice, the proportions of neutrophils, mast cells, natural killer cells and monocytes/macrophages in the aorta and peripheral blood of ApoE mice signifi¬cantly increased (P < 0.05 ) and the infiltrated mono¬cytes/ macrophages were mainly pro-inflammatory M1 monocytes/macrophages ( P < 0.05 ).The percentages of infiltrating CD3 4 T cells, Thl7 cells and Tel7 cells in the aorta, peripheral bloorl and spleen of ApoE mice significantly increased ( P < 0.05) or had an in¬creasing tendency.Conclusions At the early stage of atherosclerosis, a variety of innate immune cells and a- daptive immune cells promote the formation of inflam¬matory microenvironment, which plays an important role in the initiation of atherosclerosis.

Advances on efficacy and mechanism of vitamin D3 in adjuvant therapy of mycobacterium tuberculosis infection / 中华临床感染病杂志

Every year more than 10 million people newly infected with Mycobacterium tuberculosis (MTB) worldwide, which seriously threats human health and life. The anti-MTB infection drugs are constantly developed and updated. Vitamin D3 is a drug which can regulate the immune system, its effect on MTB infection has attracted more and more attention. This article reviews the clinical efficacy of vitamin D3 in adjuvant therapy for MTB infection, and its mechanism in regulating the innate and adaptive immune system, to provide insight for treatment of MTB infection.

Host Cell Responses to Dengue Virus / 中山大学学报(医学科学版)

@#Recent outbreak of dengue virus （DENV） in subtropics and tropics and the increasing incidence of DENV infection have seriously threatened the public health. Upon virus infection，the host cells rapidly elicit various responses through activating different signaling pathways，to fight against the invasion of DENV. On the other hand，dengue virus has evolved many strategies of escaping，antagonizing or even utilizing these host responses. This review summarizes the progress of molecular biology of DENV and the cellular responses against DENV infection，including innate immune response，adaptive immune response，cell death，autophagy，unfolded protein response，and stress granule formation.

Involvement of Vitamin D in Immune system / Монголын Анагаах Ухаан

@#Research of function of vitamin D on immune system has been studying since the study revealed that vitamin D receptor is expressed on the surface of the immune cells. 1,2-dihydroxyvitamin D3 [1,25(OH)2D], physiologically active form, can be generated through hydroxylation of 25-hydroxyvitamin D3 [25(OH)D], inactive form of vitamin D, in a liver, connecting with specific VDR make biological action. Vitamin D make different biological actions depends on connecting with different immunological cells. Some studies indicated that Vitamin D plays pivotal role in antibacterial innate immune responses through regulating reaction of the main cells as macrophages and dendritic cells. Moreover, calcitriol, the active form of vitamin D, is connected with VDRE, modulates the innate immune response through directly inducing expression of catelicithin and β-defensin as antimicrobial peptides, reducing secretion of IL-1b, IL-6, TNF-a, RANKL, COX-2 as proinflammatory cytokines and increasing production of IL-10, an anti-inflammatory cytokine. Vitamin D plays in proliferation and differentiation of T and B cells and regulates the activities of over 500 genes. Vitamin D differently impacts on per se stages of T cells’ proliferation. Vitamin D indirectly mitigates the differentiation from immature B cells to plasma B cells while it directly impacts on regulation of overloaded production of antibodies in plasma B cells. In conclusion, vitamin D modulates the innate- and adaptive immune response through regulation on activation of APCells, proliferation and differentiation of immune cells, secretion of some antibacterial peptides.

Characterization of Distinct T Cell Receptor Repertoires in Tumor and Distant Non-tumor Tissues from Lung Cancer Patients / 基因组蛋白质组与生物信息学报·英文版

T cells and T cell receptors (TCRs) play pivotal roles in adaptive immune responses against tumors. The development of next-generation sequencing technologies has enabled the analysis of the TCRβ repertoire usage. Given the scarce investigations on the TCR repertoire in lung cancer tissues, in this study, we analyzed TCRβ repertoires in lung cancer tissues and the matched distant non-tumor lung tissues (normal lung tissues) from 15 lung cancer patients. Based on our results, the general distribution of T cell clones was similar between cancer tissues and normal lung tissues; however, the proportion of highly expanded clones was significantly higher in normal lung tissues than in cancer tissues (0.021% ± 0.002% vs. 0.016% ± 0.001%, P = 0.0054, Wilcoxon signed rank test). In addition, a significantly higher TCR diversity was observed in cancer tissues than in normal lung tissues (431.37 ± 305.96 vs. 166.20 ± 101.58, P = 0.0075, Mann-Whitney U test). Moreover, younger patients had a significantly higher TCR diversity than older patients (640.7 ± 295.3 vs. 291.8 ± 233.6, P = 0.036, Mann-Whitney U test), and the higher TCR diversity in tumors was significantly associated with worse cancer outcomes. Thus, we provided a comprehensive comparison of the TCR repertoires between cancer tissues and matched normal lung tissues and demonstrated the presence of distinct T cell immune microenvironments in lung cancer patients.

Update in immune regulatory pathway of tumor necrosis factor-α-induced protein 8-like 2 / 中华危重病急救医学

The tumor necrosis factor-α-induced protein 8-like (TNFAIP8, TIPE) family is recently identified proteins consisting of four highly homologous mammalian proteins: TIPE, TIPE1, TIPE2, and TIPE3. Although the four members share similar molecular structure and function, involving effects in pathophysiological processes of inflammation, immunity, tumors, stroke, angiogenesis, and other diseases, they have individual characteristics. Many studies have shown that TIPE2 is an essential negative regulator of both innate and adaptive immunity. Up-regulation of TIPE2 expression can alleviate excessive inflammation during septic shock and maintain hemostasis of macrophages, neutrophils, dendritic cells, T cells, and B cells. In this review, we summarize the current literature for structure feature, immune function, and regulatory mechanism of TIPE2, together with its clinical significance in the pathogenesis of immune disorders of a wide array of human diseases. Understanding the basic biology of this new molecule might help us to seek novel strategies for the immunomodulation of human diseases.

Liver sinusoidal endothelial cells regulate adaptive immune tolerance in the liver / 中华肝脏病杂志

Liver sinusoidal endothelial cells are a major group of nonparenchymal cells in the liver and are involved in immunological surveillance of the liver through the expression of various scavenger receptors and pattern recognition receptors. However, in case of several physiological states, viral infections, and tumor environment, liver sinusoidal endothelial cells maintain immune tolerance in the liver through various mechanisms and cause persistent viral infection and tumor metastasis. This article reviews the mechanisms of immune tolerance of CD4 + T cells and CD8 + T cells in the liver induced by liver sinusoidal endothelial cells.

Research progress on negative regulation of adaptive immune response by NK cells / 中国免疫学杂志

Natural killer ( NK) cells are important innate effector cells and play a vital role in maintaining homeostasis through potent cytotoxic activity and cytokine production. Recent findings show that NK cells can also shape adaptive immune responses by in-fluencing a variety of immune cells. In addition to direct interactions with other immune cells,NK cells can indirectly stimulate or inhibit adaptive immune response via influencing infected cells and pathogen load. Abundant studies have highlighted the positive regulatory functions of NK cells, while their negative regulatory functions have increasingly attracted attention in recent years. Here, we review recent findings on negative regulation of adaptive immune response by NK cells, discussing the involved effector cells and function mechanism,and demonstrate how this negative regulation influences the overall outcome of adaptive immunity in infection and tumor disease.

Evasión de la respuesta inmune por virus herpes simplex / Immune evasion by herpes simplex viruses

Herpes simplex viruses and humans have co-existed for tens of thousands of years. This long relationship has translated into the evolution and selection of viral determinants to evade the host immune response and reciprocally the evolution and selection of host immune components for limiting virus infection and damage. Currently there are no vaccines available to avoid infection with these viruses or therapies to cure them. Herpes simplex viruses are neurotropic and reside latently in neurons at the trigeminal and dorsal root ganglia, occasionally reactivating. Most viral recurrences are subclinical and thus, unnoticed. Here, we discuss the initial steps of infection by herpes simplex viruses and the molecular mechanisms they have developed to evade innate and adaptive immunity. A better understanding of the molecular mechanisms evolved by these viruses to evade host immunity should help us envision novel vaccine strategies and therapies that limit infection and dissemination.

Los virus herpes simplex y humanos co-existen desde decenas de miles de años. Esta prolongada relación se ha traducido en la evolución y selección de determinantes virales para evadir la respuesta inmune y recíprocamente la evolución y selección de componentes inmunes del hospedero para limitar la infección viral y el daño que producen. Actualmente no existen vacunas para evitar la infección de estos virus o terapias que la curen. Los virus herpes simplex son neurotrópicos y permanecen latentes en neuronas de ganglios trigémino y dorsales, reactivándose esporádicamente. La mayoría de las recurrencias por virus herpes simplex son sub-clínicas y por tanto pasan inadvertidas. Aquí discutimos los pasos iniciales de la infección porvirus herpes simplex y los mecanismos moleculares que estos virus han desarrollado para evadir la respuesta inmune innata y adaptativa. Una mejor comprensión de los mecanismos moleculares evolucionados por estos virus para evadir la respuesta inmune del hospedero deberían ayudarnos visualizar nuevas estrategias para desarrollar vacunas y terapias que limiten su infección y diseminación.

Interplay between Intestinal Microbiota and Host Immune System

Whether we are aware or not, diverse microorganisms are living on almost all environmentally exposed surfaces on our body without eliciting harmful immune responses. In fact, recent understanding from numerous studies indicates that our health is highly dependent on the contribution of intestinal commensal bacteria. It appears through its symbiotic interaction with the host, which is the result of millions of years of co-evolution, the microbiota shapes the immune system. In this review, we discuss the relationship between host physiology and commensal bacteria and explore the molecular mechanisms by which the adaptive immune system is influenced by the intestinal microbiota.

Innate and adaptive immunity gene expression of human keratinocytes cultured of severe burn injury

PURPOSE: Evaluate the expression profile of genes related to Innate and Adaptive Immune System (IAIS) of human Primary Epidermal keratinocytes (hPEKP) of patients with severe burns. METHODS: After obtaining viable fragments of skin with and without burning, culture hKEP was initiated by the enzymatic method using Dispase (Sigma-Aldrich). These cells were treated with Trizol(r) (Life Technologies) for extraction of total RNA. This was quantified and analyzed for purity for obtaining cDNA for the analysis of gene expression using specific IAIS PCR Arrays plates (SA Biosciences). RESULTS: After the analysis of gene expression we found that 63% of these genes were differentially expressed, of which 77% were repressed and 23% were hyper-regulated. Among these, the following genes (fold increase or decrease): IL8 (41), IL6 (32), TNF (-92), HLA-E (-86), LYS (-74), CCR6 (- 73), CD86 (-41) and HLA-A (-35). CONCLUSIONS: This study contributes to the understanding of the molecular mechanisms underlying wound infection caused by the burn. Furthermore, it may provide new strategies to restore normal expression of these genes and thereby change the healing process and improve clinical outcome. .

Advance in immunopathogenesis for systemic lupus erythematosus / 国际儿科学杂志

Systemic lupus erythematosus is a typical autoimmune disease commonly seen in childhood, the immunnopathogenesis of which is complicated. Along with the rapid advances of immunology and molecular biology, all the associated research has found that the onset of systemic lupus erythematosus is associated with dysfunction of T cells and B cells. They focus on the break of the normal autoimmune immunity and the form of malgenic autoantibody. It is also connected with primary immunodeficiency. The dysfunction of inherent immunity contributes to the break of autoimmune and the progression of the disease.

Pathogenesis of immune dysfunction in septic and immunoregulation therapy / 临床儿科杂志

The pathogenesis of immune dysfunction in septic has been summarized in this review.Innate immune response toward pathogens is initiated by pattem recognition receptor (PRR) such as Toll-like receptor (TLR) .Inflammatory cytokines derived from innate immune response not only cause inflammatory response.but also trigger adaptive immune responses through inducing the differentiation of naive T cell into Th1, Th2, CD4~+CD25~+Foxp3~+ regulatory T cells (Treg), and Th17 cells. Adaptive immune response might suppress or enhance inflammatory response.Abnormal activation of innate/adaptive immune responses may coexist in sepsis, resulting in immune dysfunction.Logical and adequate approach of immunoregulation therapy to sepsis may be to suppress PRR persistent activation by eliminating endogenous or exogenous ligands, as well as to avoid excessive inhibition of immune responses to infection.

Avian Influenza: Should China Be Alarmed?

Avian influenza has emerged as one of the primary public health concern of the 21st century. Influenza strain H5N1 is capable of incidentally infecting humans and other mammals. Since their reemergence in 2003, highly pathogenic avian influenza A (H5N1) viruses have been transmitted from poultry to humans (by direct or indirect contact with infected birds) in several provinces of Mainland China, which has resulted in 22 cases of human infection and has created repercussions for the Chinese economy. People have been concerned whether a new pandemic will occur in the future. The eradication of pathogenic avian influenza viruses appears to be the most effective way to prevent an influenza pandemic. This paper will examine the features of H5N1, including incidence, infection, immunity, clinical management, prevention and control, and therapy in Mainland China.