|
| 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
erythrocytes | 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
(T232) | 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 | ? | ? | ? | Autoantibody production? |
|
| GYPC | GYPC-deficient erythrocytes | Protection against EBA-140-mediated invasion by P. falciparum parasites | Binding receptor-parasite protein | ? |
|
