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Equipped with his five senses, man explores the universe around him and calls the adventure Science. ~Edwin Powell Hubble, The Nature of Science, 1954
At Molecular Station Immunology Home you will find information, protocols, bioinformatics, and links on:
Immunology: Bioinformatics on Immunology
Immunology: Bioinformatics on Antigens
Control of IL-4 expression in T helper 1 and 2 cells. Related Articles
Control of IL-4 expression in T helper 1 and 2 cells.
Immunology. 2008 May 9;
Authors: Gilmour J, Lavender P
The mechanism of differentiation of naïve T cells to a variety of effector lineages, but particularly to T helper type 1 (Th1) and Th2 cells, has been the subject of intense scrutiny over the past two decades. Studies have revealed that the expression of cytokines, receptors, signalling molecules, transcription factors, DNA methylating enzymes and histone-modifying enzymes is altered during the process and has been shown to play a co-ordinated role to facilitate expression of the cytokines interleukin-4 (IL-4), IL-5 and IL-13 in Th2 cells, or interferon-gamma in Th1 cells. Regulation of IL-4 expression has been of particular interest for two main reasons: first because IL-4 acts as a growth factor for Th2 cells, and second because of its role in the induction of immunoglobulin class switching to immunoglobulin E, which plays a critical role in mediating allergic responses. Study of the pathways that promote this tissue-restricted expression of IL-4 may highlight potential areas for therapeutic intervention.
PMID: 18479352 [PubMed - as supplied by publisher]
Gpr83 expression is not required for the maintenance of intestinal immune homeostasis and regulation of T-cell-dependent colitis.
Immunology. 2008 May 9;
Authors: Toms C, Jessup H, Thompson C, Baban D, Davies K, Powrie F
Regulatory T (T(R)) cells are integral to the maintenance of intestinal homeostasis, where an intricate balance between tolerance and immunity must be maintained. Recently, studies have focused on the identification of molecules involved in the function and/or development of T(R) cells. One such molecule, the G-protein coupled receptor Gpr83, has been identified through gene expression analysis as being overexpressed within thymic and peripheral naturally arising regulatory T (nT(R)) cell populations. The aim of this study was to further define the characteristics of Gpr83 expression and to investigate the role of Gpr83 in T(R)-cell development and function through the generation and analysis of Gpr83-deficient mice. Following activation, naïve CD4(+) T cells induce Gpr83 expression in a transforming growth factor (TGF)-beta dependent manner. Rather than being a general marker of activation, Gpr83 expression could only be detected in cells also expressing forkhead/winged helix transcription factor (Foxp3), further supporting the association of Gpr83 with the regulatory cell phenotype. Mice deficient in Gpr83 expression developed normally and did not display signs of inflammatory disease. Thymic nT(R)-cell development was unaffected by a lack of Gpr83 expression and peripheral nT(R)-cell homeostasis was normal when compared with that of wild-type mice. Gpr83 expression was dispensable for the regulatory activity of nT(R) cells as Gpr83-deficient nT(R) cells could suppress the development of disease in a T-cell transfer model of colitis. These results suggest a redundant role for Gpr83 in the function of T(R) cells in this model of disease. Further studies are required to determine the role of Gpr83 in T(R)-cell biology.
PMID: 18479351 [PubMed - as supplied by publisher]
alpha1beta1 integrin and interleukin-7 receptor up-regulate the expression of RANKL in human T cells and enhance their osteoclastogenic function.
Immunology. 2008 May 13;
Authors: Gendron S, Boisvert M, Chetoui N, Aoudjit F
Activated T cells, through the production of the receptor activator of NF-kappaB ligand (RANKL) cytokine, have been implicated in the osteoclast development and bone loss that are associated with autoimmune diseases such as rheumatoid arthritis. However, the cellular pathways that regulate the expression of RANKL and the induction of osteoclasts are still unclear. In this study, we show that, in human effector CD4(+) T cells, activation of alpha1beta1 integrin and interleukin (IL)-7 receptor (IL-7R) up-regulates the expression and production of RANKL but has no effect on the production of interferon-gamma, an inhibitor of T-cell-mediated osteoclastogenesis. Thus, both alpha1beta1 integrin and IL-7R enhance the ability of these cells to induce the formation of osteoclasts from human monocytes. Furthermore, we found that simultaneous activation of effector CD4(+) T cells via alpha1beta1 integrin and IL-7R synergistically increases the production of RANKL and enhances their osteoclastogenic function. We also show that, although alpha1beta1 integrin does not protect human effector CD4(+) T cells from IL-2-withdrawal-induced apoptosis, it does enhance the pro-survival effect of IL-7, further emphasizing the importance of the alpha1beta1/IL-7R synergistic effect. Together our results identify a new function of alpha1beta1 integrin in T cells and suggest that activation of effector CD4(+) T cells through alpha1beta1 integrin and IL-7R is an important regulatory pathway in T-cell-dependent osteoclastogenesis. Further understanding of the mechanisms by which IL-7R and alpha1beta1 integrin promote T-cell-mediated osteoclastogenesis will lead to new insights into the regulatory pathways of T-cell-dependent bone resorption associated with autoimmune diseases.
PMID: 18479350 [PubMed - as supplied by publisher]
T lymphocytes in acute bacterial infection: increased prevalence of CD11b(+) cells in the peripheral blood and recruitment to the infected site.
Immunology. 2008 May 13;
Authors: Wagner C, Kotsougiani D, Pioch M, Prior B, Wentzensen A, Hänsch GM
T-cell activation, particularly of CD8(+) cells, is invariably associated with viral infections. We now provide evidence for the activation of T cells in patients with localized bacterial soft tissue infections. During acute disease we detected in the peripheral blood of these patients, small though conspicuous populations of CD4(+) CD28(+) CD11b(+) and CD8(+) CD28(+) CD11b(+) cells, indicative of an expansion of effector T cells. Moreover, we identified CD4(+) and CD8(+) cells at the infected site, in addition to highly activated polymorphonuclear neutrophils (PMN). In keeping with their role as first-line defence, PMN were preponderant, but T cells amounted to 20% of the infiltrated cells. The majority of the infiltrated T cells expressed CXCR6, a homing receptor for non-lymphoid tissue. The infiltrated T cells produced interferon-gamma (IFN-gamma), while the peripheral blood cells obtained at the same time did not. In conclusion, in response to localized bacterial infections, T cells are activated and recruited to the infected site. We propose that these T cells, e.g. by producing IFN-gamma, enhance the efficiency of the infiltrated phagocytic cells, particularly of the PMN, thereby supporting the local host defence.
PMID: 18479349 [PubMed - as supplied by publisher]
Small changes in lymphocyte development and activation in mice through tissue-specific alteration of heparan sulphate.
Immunology. 2008 May 9;
Authors: Garner OB, Yamaguchi Y, Esko JD, Videm V
We have examined the role of heparan sulphate in lymphocyte development and activation in mice by conditionally deleting the genes encoding the heparan sulphate biosynthetic enzymes N-deacetylase/N-sulphotransferase-1 and -2 (Ndst1 and Ndst2) and glucuronic acid/N-acetylglucosamine co-polymerase-1 (Ext1) in T cells and B cells, respectively. Ndst1 and Ndst2 are the only Ndst isoforms in T cells. In T-cell Ndst-deficient mice there were normal ratios of CD4(+)/CD8(+) cells in the blood, spleen and thymus, indicating no dramatic effect on development. However, Ndst-deficient T cells were hyperresponsive to low-level activation, suggesting that cell surface heparan sulphate plays a role in T-cell proliferation. The hyperresponsive state correlated with a decrease in cell surface heparan sulphate that occurs in response to activation in wild-type cells. There was a slight change in the number of developing B cells in B-cell Ext1-deficient mice, but the alteration did not cause a change in antibody production. These findings demonstrate that cell surface heparan sulphate may not play a crucial role in lymphocyte development, but can modulate the sensitivity of T cells to activation.
PMID: 18479348 [PubMed - as supplied by publisher]
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