The B7-CD28/CTLA-4 costimulatory pathways in autoimmune disease of the central nervous system

Current Opinion in Immunology

Volumn 11, Issue 6, 1999, Pages 677-683

  Anderson, David E ^a   Sharpe, Arlene H ^b   Hafler, David A ^b  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b BRIGHAM AND WOMEN S HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

B7 ANTIGEN; CD28 ANTIGEN; CYTOTOXIC T LYMPHOCYTE ANTIGEN 4;

AUTOIMMUNE DISEASE; CENTRAL NERVOUS SYSTEM DISEASE; DISEASE COURSE; HELPER CELL; HUMAN; IMMUNE RESPONSE; IMMUNOSTIMULATION; LYMPHOCYTE DIFFERENTIATION; NONHUMAN; PATHOGENESIS; REVIEW; T LYMPHOCYTE; T LYMPHOCYTE ACTIVATION;

EID: 0032706818     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(99)00036-9     Document Type: Review

References (36)

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36. -/- mice were crossed with CTLA-4-deficient mice to examine the role of CTLA-4 in Th cell differentiation. In vitro stimulation of purified, naïve, CTLA-4-deficient DO11 T cells led to Th2 differentiation whereas wild-type DO11 T cells developed into Th1 cells. In addition the T cells from the mice deficient in B7-1, B7-2 and CTLA-4 also differentiated into Th2 cells when stimulated with wild-type APCs in vitro. Administration of anti-CD28 mAb in vivo to mice deficient in B7-1, B7-2 and CTLA-4 induced IL-4 secretion but this was not seen when anti-CD28 mAb was given to wild-type mice. These data demonstrate that B7 costimulation through CD28 promotes Th2 differentiation whereas B7 engagement of CTLA-4 attenuates Th2 differentiation.