Apoptosis in brain-specific autoimmune disease

[1]  H. Hartung,et al.  Transforming growth factor-β1: A lesion-associated cytokine of the nervous system , 1995, International Journal of Developmental Neuroscience.

[2]  R. Ransohoff,et al.  Regulation and function of central nervous system chemokines , 1995, International Journal of Developmental Neuroscience.

[3]  H. Lassmann,et al.  Apoptosis of T lymphocytes in coronavirus-induced encephalomyelitis , 1995 .

[4]  K. Jellinger,et al.  Patterns of oligodendroglia pathology in multiple sclerosis. , 1994, Brain : a journal of neurology.

[5]  M. Pender,et al.  Apoptotic elimination of Vβ8.2+ cells from the central nervous system during recovery from experimental autoimmune encephalomyelitis induced by the passive transfer of Vβ8.2+ encephalitogenic T cells , 1994 .

[6]  T. Olsson.  Role of cytokines in multiple sclerosis and experimental autoimmune encephalomyelitis , 1994, European journal of neurology.

[7]  H. Hartung,et al.  Apoptotic cell death of T-lymphocytes in experimental autoimmune neuritis of the Lewis rat , 1994, Neuroscience Letters.

[8]  D. Constam,et al.  Transforming growth factor‐β2 induces apoptosis of murine T cell clones without down‐regulating bcl‐2 mRNA expression , 1994, European journal of immunology.

[9]  J. Goverman,et al.  T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis. , 1994, Science.

[10]  M. Peitsch,et al.  The apoptosis endonucleases: cleaning up after cell death? , 1994, Trends in cell biology.

[11]  I. Cohen,et al.  Shifts in the epitopes of myelin basic protein recognized by Lewis rat T cells before, during, and after the induction of experimental autoimmune encephalomyelitis. , 1993, The Journal of clinical investigation.

[12]  Y. Matsumoto,et al.  Preferential distribution of Vβ 8.2‐positive T cells in the central nervous system of rats with myelin basic protein‐induced autoimmune encephalomyelitis , 1993 .

[13]  H. Lassmann,et al.  Apoptosis of T lymphocytes in experimental autoimmune encephalomyelitis. Evidence for programmed cell death as a mechanism to control inflammation in the brain. , 1993, The American journal of pathology.

[14]  M. Lenardo,et al.  Ligand-induced apoptosis of mature T lymphocytes (propriocidal regulation) occurs at distinct stages of the cell cycle. , 1993, Leukemia.

[15]  D. McFarlin,et al.  Long-term treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-β2 , 1993, Journal of Neuroimmunology.

[16]  M. Lenardo,et al.  Propriocidal apoptosis of mature T lymphocytes occurs at S phase of the cell cycle , 1993, European journal of immunology.

[17]  A. Weinberg,et al.  Where, when, and how to detect biased expression of disease-relevant V beta genes in rats with experimental autoimmune encephalomyelitis. , 1993, Journal of immunology.

[18]  Y. Matsumoto,et al.  In situ inactivation of infiltrating T cells in the central nervous system with autoimmune encephalomyelitis. The role of astrocytes. , 1993, Immunology.

[19]  P. Marrack,et al.  Death and T Cells , 1993, Immunological reviews.

[20]  E. Sercarz,et al.  Determinant spreading and the dynamics of the autoimmune T-cell repertoire. , 1993, Immunology today.

[21]  C. Haslett,et al.  Phagocyte recognition of cells undergoing apoptosis. , 1993, Immunology today.

[22]  E. Sercarz,et al.  Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen , 1992, Nature.

[23]  B. Huber,et al.  IL-4 and IL-2 selectively rescue Th cell subsets from glucocorticoid-induced apoptosis. , 1992, Journal of immunology.

[24]  F. Sánchez‐Madrid,et al.  Prevention of experimental autoimmune encephalomyelitis by antibodies against α4βl integrin , 1992, Nature.

[25]  Y. Matsumoto,et al.  In situ demonstration of proliferating cells in the rat central nervous system during experimental autoimmune encephalomyelitis. Evidence suggesting that most infiltrating T cells do not proliferate in the target organ. , 1992, Laboratory investigation; a journal of technical methods and pathology.

[26]  M. Lenardo.  lnterleukin-2 programs mouse αβ T lymphocytes for apoptosis , 1991, Nature.

[27]  A. Cross,et al.  Adhesion-related molecules in the central nervous system. Upregulation correlates with inflammatory cell influx during relapsing experimental autoimmune encephalomyelitis. , 1991, Laboratory investigation; a journal of technical methods and pathology.

[28]  M. Pender,et al.  Apoptosis in the nervous system in experimental allergic encephalomyelitis , 1991, Journal of the Neurological Sciences.

[29]  P. Albert,et al.  Prevention and treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 1. , 1991, Journal of immunology.

[30]  J. Orenstein,et al.  Macrophage- and astrocyte-derived transforming growth factor beta as a mediator of central nervous system dysfunction in acquired immune deficiency syndrome , 1991, The Journal of experimental medicine.

[31]  W. Hickey,et al.  T‐lymphocyte entry into the central nervous system , 1991, Journal of neuroscience research.

[32]  M. Merćep,et al.  Programmed T lymphocyte death. Cell activation- and steroid-induced pathways are mutually antagonistic. , 1990, Journal of immunology.

[33]  R. Rothlein,et al.  Endothelial cell expression of the intercellular adhesion molecule-1 (ICAM-1) in the central nervous system of guinea pigs during acute and chronic relapsing experimental allergic encephalomyelitis , 1990, Journal of Neuroimmunology.

[34]  H. Schluesener.  Transforming growth factors type β 1 and β 2 suppress rat astrocyte autoantigen presentation and antagonize hyperinduction of class II major histocompatibility complex antigen expression by interferon-γ and tumor necrosis factor-α , 1990, Journal of Neuroimmunology.

[35]  A. Vandenbark,et al.  Immunization with a synthetic T-cell receptor V-region peptide protects against experimental autoimmune encephalomyelitis , 1989, Nature.

[36]  H. Wekerle,et al.  T cell receptor β chain usage in myelin basic protein‐specific rat T lymphocytes , 1989 .

[37]  D. Mason,et al.  Spontaneous recovery of rats from experimental allergic encephalomyelitis is dependent on regulation of the immune system by endogenous adrenal corticosteroids , 1989, The Journal of experimental medicine.

[38]  N. Shen,et al.  Both rat and mouse T cell receptors specific for the encephalitogenic determinant of myelin basic protein use similar V alpha and V beta chain genes even though the major histocompatibility complex and encephalitogenic determinants being recognized are different , 1989, The Journal of experimental medicine.

[39]  L. Hood,et al.  Restricted use of T cell receptor V genes in murine autoimmune encephalomyelitis raises possibilities for antibody therapy , 1988, Cell.

[40]  H. Mcdevitt,et al.  Limited heterogeneity of T cell receptors from lymphocytes mediating autoimmune encephalomyelitis allows specific immune intervention , 1988, Cell.

[41]  W. Hickey,et al.  Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo. , 1988, Science.

[42]  H. Lassmann,et al.  Cellular immune reactivity within the CNS , 1986, Trends in Neurosciences.

[43]  Y. Matsumoto,et al.  Immunohistochemical analysis of the rat central nervous system during experimental allergic encephalomyelitis, with special reference to Ia-positive cells with dendritic morphology. , 1986, Journal of immunology.

[44]  M. Sporn,et al.  Production of transforming growth factor beta by human T lymphocytes and its potential role in the regulation of T cell growth , 1986, The Journal of experimental medicine.

[45]  A. Wyllie.  Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation , 1980, Nature.