TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease. impaired B cell maturation in mice lacking BLyS

  • Immunity. 2001 Aug;15(2):289-302. doi: 10.1016/s1074-7613(01)00183-2.
J A Gross  1 ,  S R Dillon ,  S Mudri ,  J Johnston ,  A Littau ,  R Roque ,  M Rixon ,  O Schou ,  K P Foley ,  H Haugen ,  S McMillen ,  K Waggie ,  R W Schreckhise ,  K Shoemaker ,  T Vu ,  M Moore ,  A Grossman ,  C H Clegg
Affiliations
  • 1. Department of Immunology, 1201 Eastlake Avenue East, Seattle, WA 98102, USA. [email protected]
PMID: 11520463 DOI: 10.1016/s1074-7613(01)00183-2
Abstract

BLyS and APRIL have similar but distinct biological roles, mediated through two known TNF Receptor family members, TACI and BCMA. We show that mice treated with TACI-Ig and TACI-Ig transgenic mice have fewer transitional T2 and mature B cells and reduced levels of circulating immunoglobulin. TACI-Ig treatment inhibits both the production of collagen-specific Abs and the progression of disease in a mouse model of rheumatoid arthritis. In BLyS-deficient mice, B cell development is blocked at the transitional T1 stage such that virtually no mature B cells are present, while B-1 cell numbers are relatively normal. These findings further elucidate the roles of BLyS and APRIL in modulating B cell development and suggest that BLyS is required for the development of most but not all mature B cell populations found in the periphery.

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