Coevolution of hosts and microorganisms: an analysis of the involvment of cytokines in host-parasite interactions

Abstract

Parasites may employ particular strategies of eluding an immune response by taking advantage of those mechanisms that normally guarantee immunological self-tolerance. Much in the way as it occurs during the establishment of self-tolerance, live pathogens may induce clonal deletion, functional inactivation (anergy) and immunosuppression. At this latter level, it appears that certain pathogens produce immunosuppressive cytokine-like mediators or provoke the host to secrete cytokines that will compromise the anti-parasite immune response. It appears that immune responses that preferentially involve T helper 1 cells (secretors of interleukin-2-and interferon-gamma) tend to be protective, whereas T helper 2 cells (secretors of IL-4, IL-5, IL-6, and IL-10), a population that antagonizes T helper cells, mediate disease susceptibility and are involved in immunopathological reactions. Cytokines produced by T helper 2 cells mediate many symptoms of infection, including eosinophilia, mastocytosis, hyperimmunoglobulinemia, and elevated IgE levels. Administration of IL-2 and IFN-gamma has beneficial effects in many infections mediated by viruses, bacteria, and protozoa. The use of live vaccinia virus might be an avenue for the treatment of or the vaccination against infection. We have found that a vaccinia virus expressing the gene for human IL-2, though attenuated, precipitates autoimmune disease in immunodeficient, athymic mice. Thus, although T helper 1 cytokines may have desired immunostimulatory properties, they also may lead to unwarranted autoaggressive responses.

Do leprosy and tuberculosis generate a systemic inflammatory shift? Setting the ground for a new dialogue between experimental immunology and bioarchaeology

“…Deficient responses may result in increased susceptibility to pathogens, but excessive ones may result in heightened inflammation and pathologic consequences to the host (Graham et al, 2005). Immune proteins such as cytokines influence pathogenhost interactions, regulating the immune response and determining in part whether infection will result in immunological tolerance, immunity, or immunopathology (Williams et al, 1992). These proteins can be produced in excess during both innate and acquired immunity leading to immunopathology linked to two different, but not mutually exclusive, phenomena: (a) temporal protective immunity against specific pathogenic processes; and (b) pathogenic manipulation of the immune response (Graham et al, 2005).…”

“…Recent studies have also shown that microbial products disseminated throughout the body can exert systemic effects on the cellular responses (Clarke et al, 2010;Ichinohe et al, 2011;Klarstr€ om Engstr€ om et al, 2015). Immune proteins such as cytokines influence pathogenhost interactions, regulating the immune response and determining in part whether infection will result in immunological tolerance, immunity, or immunopathology (Williams et al, 1992). Deficient responses may result in increased susceptibility to pathogens, but excessive ones may result in heightened inflammation and pathologic consequences to the host (Graham et al, 2005).…”