Several diseases are associated with low physiological temperatures(27°-32°C). To determine if this association involves low temperature-induced immunosuppression, human peripheral blood leukocytes were stimulated with monoclonal anti-CD3 (αCD3), the superantigen staphylococcus enterotoxin B (SEB), a mixture of phorbol ester and calcium ionophore (TPA/CI), or the lectins ConA or PHA, and proliferation was assayed at 27°, 32° or 37°C.

Proliferative responses were suppressed at 27°C, and both diminished and delayed at 32°C. At 27°C suppression of T cell proliferation could not be obviated by TPA/CI indicating the likelihood of a block post-protein kinase C activation. This was corroborated by temperature shift-down assays wherein 18-24h at 37°C was required to bypass the block at 27°C. Furthermore, mitogenic stimulation at 27°C resulted in IL-2 secretion indicating cell activation, and that the block may involve (or be subsequent to) ligation of the IL-2 receptor.

Temperature shift-up and viability assays indicated that ConA stimulation at 27°C induced cell death, while αCD3 or SEB induced anergy. PHA also induced cell death at 27°C; however, a subpopulation of cells remained viable and some proliferation was seen when cells were shifted-up to 37°C.

These results suggest that T cell in vivo responses may differ greatly depending on the type of stimulus encountered, and the temperature at the site of activation.

(This work was supported by a grant from the Dept. Pediatrics, Univ. Miss. Med. Ctr.)