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      Apoptosis in brain-specific autoimmune disease

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          Abstract

          Recent neuropathological studies of experimental autoimmune encephalomyelitis have focused attention on the high number of cells in the lesions that show typical morphological features of apoptosis. Surprisingly, it has turned out that the vast majority of apoptotic cells are T lymphocytes and that they actually represent the antigen-specific T-cell population responsible for the induction of the disease. Taken together, these data suggest that clearance of autoimmune inflammation in the nervous system is accomplished by the destruction of the antigen-specific T-cell population within the lesions. This may explain the low level of central nervous system specific T-cell memory formation, as well as previously unexplained phenomena of ‘epitope spreading’, in autoimmune inflammation of the nervous system

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          Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo.

          W F Hickey, H. Kimura (1988)
          A crucial question in the study of immunological reactions in the central nervous system (CNS) concerns the identity of the parenchymal cells that function as the antigen-presenting cells in that organ. Rat bone marrow chimeras and encephalitogenic, major histocompatability--restricted T-helper lymphocytes were used to show that a subset of endogenous CNS cells, commonly termed "perivascular microglial cells," is bone marrow-derived. In addition, these perivascular cells are fully competent to present antigen to lymphocytes in an appropriately restricted manner. These findings are important for bone marrow transplantation and for neuroimmunological diseases such as multiple sclerosis.
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            Production of transforming growth factor beta by human T lymphocytes and its potential role in the regulation of T cell growth

            MB Sporn, LM Wakefield, R Derynck … (1986)
            This study examines the potential role of transforming growth factor beta (TGF-beta) in the regulation of human T lymphocyte proliferation, and proposes that TGF-beta is an important autoregulatory lymphokine that limits T lymphocyte clonal expansion, and that TGF-beta production by T lymphocytes is important in T cell interactions with other cell types. TGF-beta was shown to inhibit IL-2-dependent T cell proliferation. The addition of picograms amounts of TGF-beta to cultures of IL-2-stimulated human T lymphocytes suppressed DNA synthesis by 60-80%. A potential mechanism of this inhibition was found. TGF-beta inhibited IL-2-induced upregulation of the IL-2 and transferrin receptors. Specific high-affinity receptors for TGF-beta were found both on resting and activated T cells. Cellular activation was shown to result in a five- to sixfold increase in the number of TGF- beta receptors on a per cell basis, without a change in the affinity of the receptor. Finally, the observations that activated T cells produce TGF-beta mRNA and that TGF-beta biologic activity is present in supernatants conditioned by activated T cells is strong evidence that T cells themselves are a source of TGF-beta. Resting T cells were found to have low to undetectable levels of TGF-beta mRNA, while PHA activation resulted in a rapid increase in TGF-beta mRNA levels (within 2 h). Both T4 and T8 lymphocytes were found to make mRNA for TGF-beta upon activation. Using both a soft agar assay and a competitive binding assay, TGF-beta biologic activity was found in supernatants conditioned by T cells; T cell activation resulted in a 10-50-fold increase in TGF- beta production. Thus, TGF-beta may be an important antigen-nonspecific regulator of human T cell proliferation, and important in T cell interaction with other cell types whose cellular functions are modulated by TGF-beta.
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              Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen.

              P V Lehmann, T Forsthuber, A. Miller … (1992)
              Immunization with myelin basic protein (MBP) induces experimental allergic encephalomyelitis (EAE), a prototype of CD4+ T-cell mediated autoimmune disease. In rodents, MBP-reactive T-cell clones are specific for a single, dominant determinant on MBP and use a highly restricted number of T-cell receptor genes. Accordingly, EAE has been prevented by various receptor-specific treatments, suggesting similar strategies may be useful for therapy of human autoimmune disease. Here we report that in (SJL x B10.PL)F1 mice, immune dominance of a single determinant, MBP:Ac1-11, is confined to the inductive phase of EAE. In mice with chronic EAE, several additional determinants of MBP in peptides 35-47, 81-100 and 121-140 recall proliferative responses. Most importantly, reactivity to the latter determinants was also detected after induction of EAE with MBP peptide Ac1-11 alone; this demonstrates priming by endogenous MBP determinants. Thus, determinants of MBP that are cryptic after primary immunization can become immunogenic in the course of EAE. Diversification of the autoreactive T-cell repertoire due to 'determinant spreading' has major implications for the pathogenesis of, and the therapeutic approach to, T-cell driven autoimmune disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Opin Immunol
                Journal ID (iso-abbrev): Curr. Opin. Immunol
                Title: Current Opinion in Immunology
                Publisher: Published by Elsevier Ltd.
                ISSN (Print): 0952-7915
                ISSN (Electronic): 1879-0372
                Publication date PMC-release: 11 February 2002
                Publication date (Print): December 1995
                Publication date (Electronic): 11 February 2002
                Volume: 7
                Issue: 6
                Pages: 839-843
                Affiliations
                [a ]Neurological Institute, University of Vienna, Schwarzspanierstrasse 17, A-1090 Wien, Austria
                [b ]Department of Neuroimmunology, Max-Planck Institute for Phychiatry, Am Klopferspitz 18a, D-82152 Martinsried, Germany
                Article
                Publisher ID: 0952-7915(95)80057-3
                DOI: 10.1016/0952-7915(95)80057-3
                PMC ID: 7135830
                PubMed ID: 8679129
                SO-VID: 5f536e22-de1c-418d-a1f1-c1468c83bc59
                Copyright statement: Copyright © 1995 Published by Elsevier Ltd.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                Subject: Article

                ScienceOpen disciplines: Immunology
                Keywords: apc—antigen-presenting cell,cns—central nervous system,eae—experimental autoimmune encephalomyelitis,il—interleukin,mbp—myelin basic protein,tcr—t-cell receptor,tgf—transforming growth factor,v—variable
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: apc—antigen-presenting cell, cns—central nervous system, eae—experimental autoimmune encephalomyelitis, il—interleukin, mbp—myelin basic protein, tcr—t-cell receptor, tgf—transforming growth factor, v—variable

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