Secretory IgA antibody responses such as those directed against respiratory and enteric pathogens, may be impaired in protein-calorie malnutrition. In previous studies using a rat model of the mucosal immune response to cholera toxin, as little as 2 weeks of severe protein deprivation markedly impaired mucosal anti-toxin production. The present studies examined the effect of protein deprivation on lymphocyte populations which adoptively transfer either priming or suppression of a mucosal anti-toxin response from malnourished donor rats to syngeneic well nourished recipients. Either 2 or 8 weeks of protein deprivation severely impaired the development of thoracic duct lymphocytes which could transfer priming or suppression after intraduodenal priming, and impaired splenic suppressor cell development after sc priming. The abrogation of suppression by protein deprivation was dependent on the dose of sc antigen used to induce suppression. Refeeding rats after two months of protein deprivation led to recovery of both priming cell and suppressor cell function. Severe protein deprivation induces a reversible defect in both priming and suppressor cell populations; the net effect is an impaired mucosal immune response.