One of the most interesting developments in biomedical science during the past few decades has been elucidation of mechanisms mediating innate immunity. One set of innate immune mechanisms is humoral, such as complement activation.
Another set comprises pattern recognition receptors such as Toll-like receptors, which induce the production of interferons and other cytokines increasing resistance of cells such as monocytes to infections. Cytokines produced during innate immune responses are among the activators of adaptive immune responses.
Antibodies exert additive or synergistic effects with mechanisms of innate immunity. Unstable HbS clusters Band-3, a major integral red cell protein; antibodies recognize these clusters and accelerate their removal by phagocytic cells. Clustered Band 3 proteins with attached antibodies activate complement, and complement C3 fragments are oposnins recognized by the CR1 complement receptor on phagocytic cells. (Arese, et al, 2005).
A population study has shown that the protective effect of the sickle-cell trait against faciparum malaria involves the augmentation of adaptive as well as innate immune responses to the malaria parasite, illustrating the expected transition from innate to adaptive immunity. (Williams, et al, 2005).
GENETIC FACTORS INFLUENCING ADAPTIVE IMMUNITY
Humoral and cell-mediated immune responses limit malaria parasite multiplication, and many cytokines contributes to the pathogenesis of malaria as well as to the resolution of infections (Schofield and Grau, 2005). It is not surprising that genetic studies have identified several loci correlated with the severity of malaria (Frodsham and hill 2004). For example, polymorphisms at the HLA loci, which course of malaria.
In West Africa an HLA class I antigen (HLA Bw53) and an HLA class II haplotype are independently associated with protection against severe malaria. However, HLA correlations vary, depending on the genetic constitution of the polymorphic malaria parasite, which differs in different geographic locations (Frodsham and Hill, 2004).
SICKLE CELL: STIMULATION OF ADAPTIVE IMMUNITY.