Role of Interleukin‐l in Infectious Diseases

Systematic expression profiling of innate immune genes defines a complex pattern of immunosenescence in peripheral and intestinal leukocytes

“…[18][19][20][21] The salient finding is that aging is associated with decreased expression levels of TLRs, nucleotide-binding domainleucine-rich repeat receptors and functionally associated genes pointing to a quantitative decline of innate defense mechanisms, which is accompanied by an upregulation of NF-kB activity and proinflammatory cytokine release. Innate immunity and aged leukocytes P Rosenstiel et al…”

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

“…IL-lp is released from activated macrophages and a large variety of other cell types including B-lymphocytes and endothelial cells (Libby et al, 1986;Howells et al, 1988;Dinarello, 1991) and is considered to be a key mediator of the immune and inflammatory reactions to infectious and foreign agents (Dinarello, 1992). This cytokine is not only a proinflammatory substance (Stimpson et al, 1988;Hom et al, 1992;van de Loo et al, 1992) but can per se induce inflammation and tissue destruction (Pettipher et al, 1986;Chandrasekhar et al, 1990).…”

“…The ability of IL-1p to augment the neurogenic vasodilator response to capsaicin needs to be seen in context with its ability to influence the activity and function of various immune and connective tissue cells (O'Byrne et al, 1991;Dinarello, 1992). Specifically, IL-1p stimulates lymphocytes to release other cytokines (Lowenthal et al, 1986) and causes fibroblasts and synovial cells to produce prostaglandin E2 (Antoni et al, 1986;Mochan et al, 1986;O'Byrne et al, 1990b).…”

“…Another putative link between the immune system and afferent nerve fibres is interleukin-lB . This cytokine is not only a major immune mediator but is also able to initiate inflammatory reactions or to exacerbate existing inflammation (Dinarello, 1992).…”

rIL-22 as an adjuvant enhances the immunogenicity of rGroEL in mice and its protective efficacy against S. Typhi and S. Typhimurium

“…IL-6 is involved in the differentiation and proliferation of T and B cells 51 and acts in conjunction with other proinflammatory cytokines, such as TNF-a and IL-1, to initiate the early inflammatory response following infection. 52 Studies have reported that IL-6 depletion results in the exacerbation of M. avium infection 51 and also reduces the protective effect of culture filtrate protein vaccination against aerogenic M. tuberculosis infection. 53 Induction of the anti-inflammatory cytokine IL-10 54 by IL-22 may also be crucial for fine-tuning local inflammation at epithelial sites of tissue damage.…”