Function of Macrophages in Antigen Recognition by Guinea Pig T Lymphocytes

Rosenthal, Alan S.; Shevach, Ethan M.

doi:10.1084/jem.138.5.1194

Cited by 954 publications

(136 citation statements)

References 31 publications

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“…Class I1 MHC molecules are required for antigen presentation to T helper cells (36), for cytolytic T cell induction (37), and for stimulation of autologous and allogeneic mixed lymphocyte reactions (38). Other functions of class I1 MHC antigens include selection of mature class II-restricted CD4+ T lymphocytes in the thymus, class I1 MHC-incompatible graft rejection, and transmembrane signaling due to the activation of Iaexpressing cells (39).…”

Section: Discussionmentioning

confidence: 99%

Up‐regulation of class II major histocompatibility complex and intercellular adhesion molecule 1 expression on scleroderma fibroblasts and endothelial cells by interferon‐γ and tumor necrosis factor α in the early disease stage

Gruschwitz

Vieth

1997

Arthritis & Rheumatism

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Objective. To investigate the expression patterns of interferon-y (IFNy) and tumor necrosis factor a (TNFa), both of which are potent inducers of class I1 major histocompatibility complex (MHC) and intercellular adhesion molecule 1 (ICAM-I) expression, and their codistribution with HLA-DR and ICAM-1 in skin lesions, cultured fibroblasts, and peripheral blood mononuclear cells (PBMC) of systemic sclerosis (SSc) patients in different stages of disease.Methods. Investigations were carried out using immunohistochemistry studies, reverse transcriptasepolymerase chain reaction, dot-blot hybridization, and cytometric analysis. Serum levels of TNFa were determined by enzyme-linked immunosorbent assay.Results. In the early inflammatory stage of SSc, class I1 MHC and ICAM-1 expression could be detected on most endothelial cells and on fibroblasts located especially in perivascular areas surrounded by infiltrating lymphocytes, which belong to the T helper 1 phenotype expressing IFNy and TNFa. In this early disease stage, an enhanced expression of TNFa on cultured dermal fibroblasts and PBMC, as well as elevated serum titers of soluble TNFa, could be found. Matthias S. Gruschwitz, MD, Gisela Vieth: University of Erlangen-Nurnberg, Erlangen, Germany.Address reprint requests to Matthias S. Gruschwitz, MD, Department of Dermatology, University of Erlangen-Nurnberg, 91052 Exlangen, Germany.Submitted for publication December 19, 1995; accepted in revised form September 3, 1996. important in the putative autoimmune response and in the perpetuation of fibrotic processes in SSc.

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Section: Discussionmentioning

confidence: 99%

Up‐regulation of class II major histocompatibility complex and intercellular adhesion molecule 1 expression on scleroderma fibroblasts and endothelial cells by interferon‐γ and tumor necrosis factor α in the early disease stage

Gruschwitz

Vieth

1997

Arthritis & Rheumatism

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“…Apparently, these cells readily pinocytize/phagocytize this material and present it to the surrounding T cells. It is very likely that either efficient antigen processing occurs in monocytes (3940) andor additional signals are provided by these cells (41), which then stimulate the T cell repertoire that is reactive against chondrocyte membranes in patients with RA. Indeed, clonal analysis demonstrated that there was a high precursor frequency in RA T cells reactive with chondrocyte antigens.…”

Section: Discussionmentioning

confidence: 99%

Cellular immune response toward human articular chondrocytes. T cell reactivities against chondrocyte and fibroblast membranes in destructive joint diseases

Alsalameh¹,

Mollenhauer²,

Hain³

et al. 1990

Arthritis & Rheumatism

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Articular cartilage is one of the major targets in destructive joint diseases in humans. We studied cellular immune reactions against cartilage cell‐surface membranes, because it has recently been suggested that these represent possible antigenic structures, based upon the observation of autoantibodies with this specificity in certain joint diseases. A striking T cell reactivity toward chondrocyte membranes was found both in blood and synovial tissue from patients with rheumatoid arthritis. This reactivity was strongly dependent on the presence of monocytes and had all the characteristics of an antigen‐driven process. Clonal analysis demonstrated high precursor frequencies in peripheral blood T cells that were reactive against chondrocyte membranes. This response to chondrocyte membranes greatly exceeded the T cell stimulation induced by membranes from other sources such as fibroblasts or epithelial cells. In contrast to patients with rheumatoid arthritis, individuals with osteoarthritis showed a strong peripheral blood and synovial fluid T cell response not only to chondrocyte membranes, but also to fibroblast membrane material. However, there was no reactivity to epithelial cell membranes. Normal donors generally did not show significant responses to any membrane preparation. These data indicate that there is a strong T cell reactivity toward chondrocyte membranes in destructive joint disorders, and this may significantly contribute to the pathogenetic processes that occur in these diseases.

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“…Previous studies in the guinea pig (1,2) have demonstrated the requirement for genetic identity at the MHC in order for peritoneal exudate cells to present antigen effectively to primed T lymphocytes. Experiments designed to test whether similar genetic restrictions applied to antigen presentation by murine spleen cells are shown in Table I.…”

Section: Antigen Presentation By Syngeneic Semisyngeneic or Allogenmentioning

confidence: 99%

Antigen presentation in the murine T-lymphocyte proliferative response. I. Requirement for genetic identity at the major histocompatibility complex

Yano¹,

Schwartz²,

Paul³

1977

The Journal of Experimental Medicine

155

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A method is described for stimulating proliferation in primed populations of murine T lymphocytes using antigen bound to mitomycin-C-treated spleen cells. This form of antigen presentation appears to be an active process because heat-killed spleen cells are ineffective, and because genetic similarity at the major histocompatibility complex (MHC) between the responder T cells and the presenting spleen cells is required for effective interactions. At all times examined, from day 3 to day 6 of the proliferative response, syngeneic spleen cells presented antigen better to peritoneal exudate T-lymphocyte-enriched cells (PETLES) than semisyngeneic F(1) spleen cells, which in turn could present antigen better than totally allogeneic spleen cells. Spleen cell mixing experiments demonstrated that these genetic restrictions were not the result of suppression by the ongoing mixed lymphocyte reactions (MLR) in the allogeneic and F(1) cases. Furthermore, incompatibility at the Mls locus generated a strong MLR but failed to prevent antigen presentation if the spleen cells and PETLES were compatible. Genetic mapping studies demonstrated that compatibility at only the I-A subregion of the MHC was sufficient for effective presentation of the antigen, dinitrophenylated ovalbumin. Compatibility at only the K region, or the K and D regions was not sufficient. These results support the concept that functional activation of primed, proliferating T lymphocytes requires the participation of gene products coded for by the I region of the MHC. This conclusion is consistent with a growing body of evidence which suggests that most T cells recognize antigen in association with MHC gene products.

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Function of Macrophages in Antigen Recognition by Guinea Pig T Lymphocytes

Cited by 954 publications

References 31 publications

Up‐regulation of class II major histocompatibility complex and intercellular adhesion molecule 1 expression on scleroderma fibroblasts and endothelial cells by interferon‐γ and tumor necrosis factor α in the early disease stage

Up‐regulation of class II major histocompatibility complex and intercellular adhesion molecule 1 expression on scleroderma fibroblasts and endothelial cells by interferon‐γ and tumor necrosis factor α in the early disease stage

Cellular immune response toward human articular chondrocytes. T cell reactivities against chondrocyte and fibroblast membranes in destructive joint diseases

Antigen presentation in the murine T-lymphocyte proliferative response. I. Requirement for genetic identity at the major histocompatibility complex

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