HLA-B and parasitic infectious disease: Consistent with this hypothesis, it has been proposed that HLA‐B‐mediated protection to malaria acts via immune inhibition through KIR receptors (B53 being a Bw4 inhibitory ligand to KIR) rather than via (or in addition to) pre‐erythrocytic T‐cell immune responses (Digitale et al. 2021; Norman et al. 2013), whereas HLA class II molecules are thought to trigger antibody‐restricted immunity across all stages of the parasitic infection (Fiorillo et al. 2017; Medhasi and Chantratita 2022; Meyer et al. 2006).