A common feature of autoimmunity is the presence of autoantibodies (AAb). Two types of AAb have beendescribed: the ‘pathogenic’ AAb, associated with autoimmune diseases (AID), and the so-called ‘natural’ AAb. Thelatter are present in all normal individuals and have been postulated to play a major role as a first defensive barrierof the organism. Both the ‘pathogenic’ and the ‘natural’ AAb can be detected at higher frequencies among individualsexposed to viral, bacterial and parasitic infections. The malaria associated AAb do not seem to result from ageneralised polyclonal B-cell activation (PBA), have specificities that may differ according to the degree of clinicalimmunity and do not seem to be pathogenic. Malaria may offer a protective effect against AID, by diminishing itsseverity or by either preventing or retarding its expression. AAb could also participate in the immune protectionagainst malaria, and this could happen in several ways: (i) AAb directed to modified Ag expressed on the red bloodcell (RBC) membrane during parasitisation and (ii) AAb reactive with crypto- or neo-Ag revealed on both normaland infected RBC membranes, by destroying infected, and also normal, erythrocytes; (iii) anti-idiotype AAb specificof the binding site of anti-merozoite Ab, which would mimic the parasite ligand for the RBC receptor, by competingwith parasites and blocking RBC invasion; (iv) AAb cross-reactive with parasite material — such as nuclear orcytoskeleton Ag — having a direct parasiticide activity; (v) the natural AAb network, through its ‘anti-bacterial firstdefense barrier’; and finally (vi) anti-phospholipid (PL) AAb, by neutralizing the pathogenic properties of parasite-derived PL. Finally, in view of currently available knowledge, it is concluded that, since AAb are not alwayspathogenic, the price for an ‘autoimmunity-mediated’ protection in malaria would not necessarily be immunopathol-ogy and clinical autoimmunity, and a protective role of AAb could be exerted with no danger to the host.