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*
Laboratory of Rheumatology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland;
Department of Pathology, School of Medicine, Geneva, Switzerland; and
Division of Rheumatology, University Hospital of Geneva, Geneva, Switzerland
Leptin is produced almost exclusively by adipocytes and regulates
body weight at the hypothalamic level. In addition, recent studies
showed that leptin plays an important role in T lymphocyte responses.
To examine the role of leptin in Ag-induced arthritis, the development
of joint inflammation was assessed in immunized leptin-deficient mice
(ob/ob), +/?, and wild-type mice (+/+) following the
administration of methylated BSA into the knees. The results showed
that ob/ob mice developed less severe arthritis compared
with control mice. The levels of IL-1
and TNF-
mRNA in the
synovium of arthritic knees were lower in ob/ob than in
+/? mice. In vitro Ag-specific T cell proliferative responses were
significantly decreased in ob/ob mice with lower IFN-
and higher IL-10 production, suggesting a shift toward a Th2-type
response in ob/ob mice. The serum levels of
anti-methylated BSA Abs of any isotype were significantly decreased
in arthritic ob/ob mice compared with controls.
Essentially identical results were obtained in db/db
mice, which lack the expression of the long isoform of leptin receptor.
By RT-PCR, we observed that B lymphocytes express leptin receptor mRNA,
indicating that in addition to its effect on the cellular response,
leptin may exert a direct effect on B cell function. In conclusion,
leptin contributes to the mechanisms of joint inflammation in
Ag-induced arthritis by regulating both humoral and cell-mediated
immune responses.
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G Palmer and C Gabay A role for leptin in rheumatic diseases? Ann Rheum Dis, October 1, 2003; 62(10): 913 - 915. [Full Text]
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M Bokarewa, D Bokarew, O Hultgren, and A Tarkowski Leptin consumption in the inflamed joints of patients with rheumatoid arthritis Ann Rheum Dis, October 1, 2003; 62(10): 952 - 956. [Abstract] [Full Text]
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 A. M. Madiehe, T. D. Mitchell, and R. B. S. Harris Hyperleptinemia and reduced TNF-alpha secretion cause resistance of db/db mice to endotoxin Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2003; 284(3): R763 - R770. [Abstract] [Full Text] [PDF]
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