Ineffective cellular interaction and interleukin 2 deficiency causing T cell defects in human allogeneic marrow recipients early after grafting and in those with chronic graft-versus-host disease

• Published in: Transplantation proceedings Vol. 16; no. 6; p. 1470
• Main Authors: Tsoi, M S, Mori, T, Brkic, S, Dobbs, S, Gillis, S, Santos, E, Thomas, E D, Storb, R
• Format: Journal Article
• Language: English
• Published: United States 01.12.1984
• Subjects: Bone Marrow Transplantation; Graft vs Host Disease; Histocompatibility Testing; Humans; Immunity, Cellular; Interleukin-2 - analysis; Lymphocyte Activation; Monocytes - immunology; T-Lymphocytes - immunology
• ISSN: 0041-1345

Impairment in T cell proliferation in response to E. coli and in CML to unrelated alloantigens was usually observed in patients early after marrow grafting and persisted in long-term patients with chronic GVHD but not in those without chronic GVHD. We analyzed various cellular functions in the pathway of T cell activation and found that in patients with immunodeficiency, (1) their M phi usually could process and present antigens to normal T cells, (2) their T cells did not proliferate even in the presence of normal antigen-pulsed M phi, (3) IL-2 production by T cells was deficient, and (4) exogenous IL-2 restored CML activity in cells of most patients early after grafting but not in cells of most patients with chronic GVHD. Therefore, failure to induce proliferation and cytotoxicity in T cells of marrow recipients is not likely due to M phi defects but because of ineffective communication among T cell subsets, probably related to impaired IL-2 production and/or unresponsiveness to IL-2.