TY - JOUR
T1 - Pathogenic mechanisms in autoimmune diseases
AU - Rose, Noel R.
N1 - Funding Information:
The author thanks Drs. Gordon Ada and David Neumann for reviewing this manuscript and Mrs. Hermine Bongers for her editorial assistance. The investigations on myocarditis and thyroiditis were supported by NIH Grants HL-33878 and AR-31632.
PY - 1989/11
Y1 - 1989/11
N2 - Autoimmunity may be initiated by a variety of mechanisms involving changes in autologous antigens or alterations in immune regulation. Autoimmune disease, the pathological consequence of an autoimmune response, depends principally upon the stimulation of helper/inducer T cells reactive with self-antigens. Such T cells direct the quantity and quality of the immune response by influencing the mixture of interleukins produced. Autoantibodies react with accessible cells and mediate injury directly or indirectly. Delayed hypersensitivity reactions indirectly damage tissues through the agency of lymphokines. Cytotoxic T cells penetrate tissue spaces and attack cells bearing requisite surface antigens complexed with the appropriate major histocompatibility complex product. Macrophages and NK cells, activated by lymphokines, have potential to augment tissue damage. These several mechanisms do not operate in isolation; rather, multiple processes act in unison in most autoimmune diseases.
AB - Autoimmunity may be initiated by a variety of mechanisms involving changes in autologous antigens or alterations in immune regulation. Autoimmune disease, the pathological consequence of an autoimmune response, depends principally upon the stimulation of helper/inducer T cells reactive with self-antigens. Such T cells direct the quantity and quality of the immune response by influencing the mixture of interleukins produced. Autoantibodies react with accessible cells and mediate injury directly or indirectly. Delayed hypersensitivity reactions indirectly damage tissues through the agency of lymphokines. Cytotoxic T cells penetrate tissue spaces and attack cells bearing requisite surface antigens complexed with the appropriate major histocompatibility complex product. Macrophages and NK cells, activated by lymphokines, have potential to augment tissue damage. These several mechanisms do not operate in isolation; rather, multiple processes act in unison in most autoimmune diseases.
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U2 - 10.1016/0090-1229(89)90065-2
DO - 10.1016/0090-1229(89)90065-2
M3 - Article
C2 - 2676277
AN - SCOPUS:0024455105
SN - 0090-1229
VL - 53
SP - S7-S16
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
IS - 2
ER -