T Lymphocyte Subpopulations in Anorexia Nervosa and Refeeding

Department of Immunology, King's College School of Medicine and Dentistry, London, United Kingdom.
Clinical Immunology and Immunopathology 04/1997; 82(3):282-9. DOI: 10.1006/clin.1996.4310
Source: PubMed


Several studies have addressed the question of the effects of starvation on immune function and changes in lymphocyte subsets. Patients with anorexia nervosa are severely malnourished, but there have been few studies of immune parameters in this group. For this reason, phenotypic markers of T cell function and activation were studied in 20 severely underweight patients with anorexia nervosa and again after a period of refeeding. The most significant finding was a reduction in the percentage and absolute number of CD8+ T cells in patients with anorexia, the result of a marked reduction in memory (CD45RO+RA-) CD8 cells. A tendency for recovery in numbers of this subset was seen after refeeding. A decreased memory:maive cell ratio was also seen among CD4 cells, but was less marked. Subtle abnormalities in activated CD4 and CD8 cells were also found in the patient group at the initial sampling, but did not follow any clear pattern. These findings indicate that starvation in anorexic patients is accompanied by a large change in memory CD8 T cells. It may be speculated that this relates to the perceived lack of symptomatic common viral infections in underweight anorexic patients and their return with the recovery of weight.

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    • "For example, it is not yet clear whether a deficit in energy intake per se or deficit in an individual macronutrient (e.g., protein; Norris et al., 1990) or micronutrient (e.g., zinc; Hosea, Rector, & Taylor, 2004) is responsible. A role for raised circulating cortisol has been proposed to account for decreased circulating T-lymphocyte populations in anorexia nervosa patients during starvation (Mustafa et al., 1997) and low lymphoid-organ cell numbers in rats during energy restriction (Fraker, King, Laakko, & Vollmer, 2000). Indeed, lower CD4 + CD8 + pre-T cells in the thymus of zinc-deficient and energy-deficient mice has been attributed to greater apoptosis resulting from elevated circulating cortisol (Hosea et al.; King et al., 2002). "
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    ABSTRACT: Several studies have addressed the question of starvation effects on immune function by means of changes in lymphocyte subsets, cytokine induction or lymphocyte activation. Anorexia nervosa (AN) patients are severely malnourished and contradictory results have been obtained regarding the accompanying immunodeficiency, including its assignation as a part of the primary nervous disorder. In the present work, an extensive immunological function examination was carried out on 40 AN patients who were compared with a control group of 14 healthy girls. The AN patients were also classified according to their nutritional status (by the Body Mass Index: BMI), this being critical for a better understanding of these secondary immunodeficiency bases. Moreover, another immune system study was performed on five patients after refeeding. Lymphocyte subsets and function, cytokine induction and peripheral blood concentrations, and innate as well as humoral immunity were evaluated. Deregulation in the cytokine network, owing to the interaction of the central nervous (CNS) and immune systems, seems to be the initial immune alteration in AN immunodeficiency but it has not been disproved that the immunodeficiency is a direct consequence of the original psychiatric perturbation. Spontaneous high levels of circulating interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) have been observed; this is probably one of the causes of the anomalies found in the T-cell subpopulations (mainly the naive CD4+CD45RA+ reduction and the cytotoxic CD8+ increase) and T-cell activation status (mainly the down-regulation of the CD2 and CD69 activation pathways). This finally leads to an impairment, not only in T-cell function but also in T-cell to B-cell co-operation. The AN specificity of these results is confirmed by the fact that these immune alterations improve after refeeding and when nutritional status becomes less critical, which also suggests that AN immunodeficiency is indeed secondary to malnutrition.
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