Constitutive expression of BCL-X(L) in the T lineage attenuates collagen-induced arthritis in Bcl-X(L) transgenic mice.

Chen Y, Rosloniec E, Price J, Boothby M, Chen J
Arthritis Rheum. 2002 46 (2): 514-21

PMID: 11840455 · DOI:10.1002/art.10128

OBJECTIVE - To determine if inhibition of T cell apoptosis through constitutive expression of Bcl-X(L) in the T lineage influences inflammatory arthritis in the mouse collagen-induced arthritis (CIA) model.

METHODS - The incidence and severity of arthritis were quantified in Bcl-X(L) transgenic mice and nontransgenic littermates after immunization with type II collagen (CII). To correlate T cell responses with disease phenotype, antigen-specific T cell proliferation was measured by (3)H-thymidine incorporation. Apoptosis and cell cycle progression were analyzed by flow cytometry using propidium iodide. Production of CII-specific interferon-gamma (IFNgamma), interleukin-5 (IL-5), and IL-10 was determined by enzyme-linked immunosorbent assay.

RESULTS - Disease severity in CIA was significantly attenuated in Bcl-X(L) transgenic mice compared with their nontransgenic littermates. Inhibition of CIA was associated with decreased T cell apoptosis, delayed cell cycle progression, and reduced IFNgamma production.

CONCLUSION - Rather than promoting inflammation, inhibition of apoptosis by expression of the Bcl-X(L) protein in the T lineage attenuates disease progression in CIA, probably through inhibition of IFNgamma production.

MeSH Terms (15)

Animals Apoptosis Arthritis, Experimental bcl-X Protein Cell Cycle Cell Lineage Gene Expression Interferon-gamma Lymphoid Tissue Mice Mice, Inbred DBA Mice, Transgenic Proto-Oncogene Proteins c-bcl-2 T-Lymphocytes Transgenes

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