Table 1.

Functional evidence of T cell involvement in experimental crescentic GNa

Models involving organ-specific autoimmunity
    EAGMiceTCR-deficient mice do not develop GN even after passive transfer of anti-GBM antibodies (5)
RatsCD4 depletion attenuates injury in BN rats (4)
CD8 depletion attenuates injury in Wky rats (9)
Models involving systemic autoimmunity
    MRL/lpr lupusMiceAnti-CD4 treatment suppresses autoimmunity and GN (6)
α/βTCR T cell–deficient mice are partially susceptible to disease (15,16), and δ/γ T cell deficiency augments GN (15)
    NZB/NZW F1 lupusMiceAnti-CD4 treatment prevents autoimmunity and GN (7)
    NZM2338 lupusMiceTransfer of CD4+CD25+ Treg does not suppress proliferative GN (14)
    (SWR×NZB)F1MiceTransfer of CD4+CD25+ Treg suppresses autoantibodies and GN (12)
    BXSB-Yaa lupusMiceα/β TCR T cell deficiency prevents autoimmunity and GN (17)
Models initiated by heterologous planted antigens
    NTNMiceCD4 T cell deficiency prevents disease (2)
CD8 T cell deficiency exacerbates disease (2)
Anti-CD4 antibody prevents disease (3)
α/β and γ/δ T cell contribute to GN (18)
Transfer of CD4+CD25+ Treg suppresses GN (13)
RatsAnti-CD4 antibody attenuates disease (1)
CD4 depletion in the effector phase of injury attenuates GN (8)
Anti-CD8 antibody attenuates macrophage accumulation and disease in WKY rats (10,11)
  • a EAG, experimental autoimmune anti–glomerular basement membrane glomerulonephritis; GBM, glomerular basement membrane; GN, glomerulonephritis; NTN, nephrotoxic serum nephritis; TCR, T cell receptor; Treg, T regulatory cells.