Journal
JOURNAL OF IMMUNOLOGY
Volume 177, Issue 1, Pages 169-176Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.1.169
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Funding
- NHLBI NIH HHS [HL 67314, P01 HL067314] Funding Source: Medline
- NIAID NIH HHS [AI 51445, P30 AI051445] Funding Source: Medline
- NIA NIH HHS [R01 AG025150, R01 AG025150-02] Funding Source: Medline
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The thymus is a lymphoid organ that selects T cells for release to the peripheral immune system. Unfortunately, thymopoiesis is highly susceptible to damage by physiologic stressors and can contribute to immune deficiencies that occur in a variety of clinical settings. No treatment is currently available to protect the thymus from stress-induced involution. Leptin-deficient (ob/ob) mice have severe thymic atrophy and this finding suggests that this hormone is required for normal thymopoiesis. In this study, the ability of leptin to promote thymopoiesis in wild-type C57BL/6 and BALB/c mice, as well as in leptin-deficient (ob/ob) and endotoxin-stressed (Escherichia coli LPS) mice, was determined. Leptin administration induced weight loss and stimulated thymopoiesis in ob/ob mice, but did not stimulate thymopoiesis in wild-type C57BL/6 nor BALB/c mice. In endotoxin-stressed mice, however, leptin prevented LPS-induced thymus weight loss and stimulated TCR alpha gene rearrangement. Coadministration of leptin with LPS blunted endotoxin-induced systemic corticosterone response and production of proinflammatory cytokines. Thus, leptin has a selective thymostimulatory role in settings of leptin deficiency and endotoxin administration, and may be useful for protecting the thymus from damage and augmenting T cell reconstitution in these clinical states.
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