TY - JOUR
T1 - Deficient T-cell mitogen response in murine experimental autoimmune myasthenia gravis
T2 - A defect in the adherent cell population
AU - Christadoss, Premkumar
AU - Dauphinee, Michael
AU - Lindstrom, Jon
AU - Dang, Howard
AU - Fernandes, Gabriel
AU - Talal, Norman
N1 - Funding Information:
’ Supported by grants from the Muscular Dystrophy Association and the Veterans Administration. *To whom correspondence should be addressed: Department of Medicine, Division of Clinical Immunology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr. San Antonio, Tex. 78284.
PY - 1983/7/15
Y1 - 1983/7/15
N2 - T-Lymphocyte number and functions are often reduced, while B-lymphocyte function is often increased in patients with autoimmune disorders. To study the mechanisms responsible for these T-cell malfunctions in autoimmunity we adapted the murine experimental autoimmune myasthenia gravis (EAMG) model. Splenocytes from C57BL/6 mice immunized with acetylcholine receptors (AChR) in complete Freund's adjuvant (CFA) produced approximately half the amount of concanavalin A (Con A)-induced interleukin 2 (IL-2) as did splenocytes of CFA-inoculated controls. Further, AChR plus CFA-immunized splenocytes showed a marked reduction in T-cell proliferative responses induced by Con A or phytohemagglutinin when compared with CFA-inoculated controls. By contrast, lipopolysaccharide-induced B-cell function is preserved. Deficient Con A splenic T-cell response is seen early after secondary inoculation with CFA or AChR in CFA. T-Cell recovery occurs in CFA-inoculated mice but not in AChR plus CFA-inoculated mice. Defective Con A splenic T-cell response seen early after secondary immunization with CFA or AChR in CFA is due to the presence of a defective splenic adherent cell population. Moreover, defective Con A splenic T-cell response seen after established autoimmunity to AChR in EAMG is also due to the presence of a defective splenic adherent cell population.
AB - T-Lymphocyte number and functions are often reduced, while B-lymphocyte function is often increased in patients with autoimmune disorders. To study the mechanisms responsible for these T-cell malfunctions in autoimmunity we adapted the murine experimental autoimmune myasthenia gravis (EAMG) model. Splenocytes from C57BL/6 mice immunized with acetylcholine receptors (AChR) in complete Freund's adjuvant (CFA) produced approximately half the amount of concanavalin A (Con A)-induced interleukin 2 (IL-2) as did splenocytes of CFA-inoculated controls. Further, AChR plus CFA-immunized splenocytes showed a marked reduction in T-cell proliferative responses induced by Con A or phytohemagglutinin when compared with CFA-inoculated controls. By contrast, lipopolysaccharide-induced B-cell function is preserved. Deficient Con A splenic T-cell response is seen early after secondary inoculation with CFA or AChR in CFA. T-Cell recovery occurs in CFA-inoculated mice but not in AChR plus CFA-inoculated mice. Defective Con A splenic T-cell response seen early after secondary immunization with CFA or AChR in CFA is due to the presence of a defective splenic adherent cell population. Moreover, defective Con A splenic T-cell response seen after established autoimmunity to AChR in EAMG is also due to the presence of a defective splenic adherent cell population.
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U2 - 10.1016/0008-8749(83)90077-1
DO - 10.1016/0008-8749(83)90077-1
M3 - Article
C2 - 6223709
AN - SCOPUS:0020573291
SN - 0008-8749
VL - 79
SP - 358
EP - 366
JO - Cellular Immunology
JF - Cellular Immunology
IS - 2
ER -