|Factor||Evolutionary modification||Resistance mechanism to malaria||Modified immunological pathway||Possible role in rheumatoid arthritis pathogenesis|
|Duffy antigen||Duffy-negative allele||Lack of expression of chemokines receptor||Chemokines sink||Amplification of immune response and lack of chemokines depuration |
|-globin||Sickle hemoglobin||Suppression of parasite growth in red cells and enhanced splenic clearance of parasitized |
|Reduced parasite cytoadherence||Unknown. |
Increased expression of VCAM-1, E-selectin, and ICAM-1?
Decrease of immune complexes clearance by asplenia.
|FcγIIB||Substitution of |
threonine for isoleucine
at position 232
in the transmembrane
domain of FcγRIIB
|Increased clearance of malarial parasites||Phagocytosis of plasmodium falciparum-infected erythrocytes. Differentiation of B lymphocytes ||The abnormal function leads to an increase in immune reactivity mainly mediated by B lymphocytes|
|CR1||Polymorphisms of CR1 are involved in the amount of protein expression in the red cell membrane.||Reduced ability of P. falciparum-infected CR1-deficient red blood cells to form rosettes||Reduced ability of P. falciparum-infected CR1-deficient red blood cells to form rosettes, and less severe disease||CR1 is a complement regulatory protein, responsible for removing immune complexes from the circulation. Decreased of immune complexes clearance|
|NK1.1(−) andNK1.1(+) |
subsetsofTCR (int) cells
|GYPC||GYPC-deficient erythrocytes ||Protection against EBA-140-mediated invasion by P. falciparum parasites ||Binding receptor-parasite protein||?|