T lymphopaenia in relation to body mass index and TNF‐α in human obesity: adequate weight reduction can be corrective

Abstract

OBJECTIVE: Although individuals with obesity are susceptible to infection, the underlying causes have not been fully identified. To investigate whether obesity affects immunity, we studied subjects with isolated obesity. DESIGN AND SUBJECTS: Thirty‐four obese persons from our outpatient obesity clinic and 50 nonobese healthy control subjects were studied. The effects of weight reduction were evaluated in obese subjects on a very‐low‐energy diet. We examined blastogenic response, lymphocyte subsets, circulatory TNF‐α, soluble TNF‐α receptor 1, soluble TNF‐α receptor 2, and in vitro TNF‐α production in obesity. MEASUREMENTS: Lymphocyte subsets were analysed with flowcytometry. TNF‐α and soluble TNF receptors levels were assayed using commercially available enzyme‐linked immunosorbent assay kits. RESULTS: Blastogenic responses to phytohemagglutinin or concanavalin A of T cells, CD3+, CD4+, CD8+, CD4+CD45RO+, and TCR αβ T cells were significantly diminished in obese subjects. Strong negative correlations were observed between TCR αβ and body weight and BMI in obese subjects. Circulatory levels of TNF‐α, soluble TNF‐α receptors, and in vitro TNF‐α production were significantly increased compared to nonobese subjects. In obese subjects, there were significant positive correlations between serum levels of TNF‐α and waist‐hip ratio, serum levels of soluble TNF‐α receptor 1 and body weight, soluble TNF‐α receptor 2 and BMI, and soluble TNF‐α receptor 2 and waist‐hip ratio. The T cell responses and previously reduced non‐CD8 T cell subsets were increased significantly following weight reduction. CONCLUSIONS: Our results suggest that subsets of T cell populations and their function may be reduced in human obesity, and that this may be related, at least in part, to the elevated TNF‐α production. Furthermore, this T cell dysfunction can be recovered by adequate weight reduction.