Response to influenza vaccination in community and in nursing home residing elderly: relation to clinical factors.

Intramuscular (IM) influenza vaccines are about 50% effective in preventing respiratory illness among the elderly. The aim of this study was to identify factors associated with immune response to influenza vaccination among nursing home and community-residing elderly. 114 nursing home (NHE) and 62 community residing elderly (CE) were vaccinated with a commercial IM vaccine. Serum antibodies were evaluated by HIA, and the impact of subjects' clinical characteristics on seroconversion was determined. Factors that were associated with low seroconversion among NHE, included: type II diabetes [for B/Harbin: p=0.044, OR 0.12, (CI: 0.015-0.94)], and antibody titer prior to vaccination A/(H1N1): p=0.03, OR 2.38, (CI: 1.09-5.22); A/(H3N2): p=0.015, OR 2.68 (CI: 1.22-5.92), B/Harbin: p=0.057, OR 4.46 (CI: 0.96-20.85)]. Factors that were associated with lower seroconversion CE elderly, included older age [A/(H1N1): p=0.008, OR 0.846, (CI 0.75-0.96), B/Harbin: p=0.016, OR 0.812, (CI:0.69-0.96)], and antibody titer prior to vaccination A/(H1N1): p=0.029, OR 4.08, (CI: 1.16-14.37); A/(H3N2): p<0.0001, OR 11.495 (CI: 3.18-41.55)]. There was no significant difference in seroconversion between nursing home residing elderly and community elderly. We conclude that Type-II diabetes and antibody titer>1:40 prior to vaccination are associated with reduced response to the influenza vaccination in nursing home elderly.

Sustained exposure to bacterial antigen induces interferon-gamma-dependent T cell receptor zeta down-regulation and impaired T cell function.

T cell antigen receptor zeta chain down-regulation and impaired in vitro T cell function have been described in cancer and autoimmune and infectious diseases. However, the immunological basis for this phenomenon is unknown. Sustained exposure to antigen and chronic systemic inflammation, factors shared by the various pathologies, might account for this phenomenon. We developed an in vivo experimental system that mimics these conditions and show that sustained exposure of mice to bacterial antigens was sufficient to induce T cell antigen receptor zeta chain down-regulation and impair T cell function, provided an interferon-gamma-dependent T helper type 1 immune response developed. This indicates zeta chain down-regulation could be a physiological response that attenuates an exacerbated immune response. However, it can act as a 'double-edged sword', impairing immune responses to chronic diseases.