Literature search services are currently unavailable. During our hosting provider's UPS upgrade we experienced a hardware failure and are currently working to resolve the issue.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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

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.

Pubmed ID: 11520463


  • Gross JA
  • Dillon SR
  • Mudri S
  • Johnston J
  • Littau A
  • Roque R
  • Rixon M
  • Schou O
  • Foley KP
  • Haugen H
  • McMillen S
  • Waggie K
  • Schreckhise RW
  • Shoemaker K
  • Vu T
  • Moore M
  • Grossman A
  • Clegg CH



Publication Data

August 24, 2001

Associated Grants


Mesh Terms

  • Animals
  • Antibody Formation
  • Arthritis, Rheumatoid
  • Autoantibodies
  • Autoimmune Diseases
  • B-Cell Activation Factor Receptor
  • B-Lymphocytes
  • Cell Differentiation
  • Cell Lineage
  • Collagen
  • Homozygote
  • Immunoglobulins
  • Membrane Proteins
  • Mice
  • Mice, Transgenic
  • Phenotype
  • Receptors, Tumor Necrosis Factor
  • Transmembrane Activator and CAML Interactor Protein