The required interaction between monocytes and peripheral blood T lymphocytes (T‐PBL) upon activation via CD2 or CD3. Role of HLA class I molecules from accessory cells and the differential response of T‐PBL subsets

摘要

AbstractPreviously, we have shown that paraformaldehyde‐fixed monocytes are able to fully complement, in terms of 3HdThd incorporation, a primary stimulus delivered to purified T cells by monoclonal antibodies (mAb) reacting with CD3 or CD2 molecules. Here, we show that depending on the stimulus used (CD3 mAb or different pairs of CD2 mAb) HLA class I molecules from monocytes are directly involved in complementary signals provided to T cells. This was evidenced by the following observations: (a) mAb reacting with the heavy or light chain of class I molecules, or their Fab fragments, completely blocked proliferation of peripheral blood lymphocytes (PBL) activated by CD3 mAb; (b) mAb against the heavy chain of HLA class I but not against p2‐microglobulin partially blocked (= 50) PBL activation by the CD2 "GT2 + T1l1" mAb pair but did not block activation by CD2 "D66 + T111" mAb; (c) this pattern of inhibition was observed when anti‐class I mAb were used in the soluble phase or when they were bound to monocytes subsequently fixed with paraformaldehyde and cultivated with purified autologous T cells; (d) fixed monocytes are able to restore interleukin (IL) 2 receptor expression on purified T cells stimulated by CD3 mAb or CD2 "GT2 + T111contrary to anti‐HLA class I mAb‐pretreated monocytes. The inhibitory effects of anti‐HLA class I mAb bound to monocytes were not found to be reversed by recombinant IL2 or recombinant IL1. We assume that HLA class I would be involved in two or more signals delivered to T cells by monocytes, the requirement in those signals depending on the initial stimulus applied to T cells. Transmission of one signal would require a conformation of the HLA molecule inhibitable by both or either anti‐heavy and anti‐light chain mAb. In searching for the counterpart to the accessory cell HLA class I molecule, we found that both CD4+and CD8+cells responded to stimulation via CD2 or CD3 mAb. However, within the CD4 subsets, the CD4+w29−subset did not respond while the reciprocal subset did. This was not due to a lack of IL2, as shown by adding rIL2. Since the CD4+w29−subset is committed to the induction of suppression while the reciprocal subset to the induction of help, one can forsee how the immune response could develop in one direction or the other depending on the type of interaction that occurs durin