Erythrocyte Immune Complex Binding Capacity In Children With Severe Plasmodium Falciparum Malaria And Those With Uncomplicated Malaria

Abstract

The term Immune Complex denotes a reaction product resulting from the interaction between an antigen and an antigen-specific or non-specific antibody and is used synonymously with antigen-antibody complex. Immune complex formation is a highly efficient mechanism of host defence directed to eliminate antigens and favour an adequate immune response. Both self and non-self or exogenous antigens can trigger formation of immune complexes. Once formed, the immune complexes are usually removed from circulation via erythrocyte complement receptors, which mop them up in a process known as immune adherence. If this mechanism fails, immune complexes can accumulate and become deleterious to the host. It has been postulated that formation of immune complexes during infection with P. falciparum could aggravate the pathology of malaria, contributing to its severity if the host does not have an effective clearance mechanism to prevent their deposition in vital organs. The purpose of the present study was to investigate in vitro the differences in immune complex binding capacities of erythrocytes from naturally infected non-immune children from malaria endemic area and correlate these with the uncomplicated disease state. Children with severe malaria or cerebral malaria (coma) were compared to controls of the same age and gender who had uncomplicated malaria. Using cytofluorometric techniques, erythrocyte immune complex binding capacities were elucidated during an episode of acute malaria as well as during a subsequent two-month follow-up for both groups. The results from this study indicate that: (i) The erythrocytes immune complex binding capacities were lower in cases of acute malaria especially in cases of severe malarial anaemia and significantly exhibited increased immune complex binding capability two months after treatment (p<O.0005). (ii) The erythrocyte immune complex binding capacities were comparably higher in cerebral malaria cases than in severe malarial anaemia (p<O.0005). Similar trend was noticed in the symptomatic control groups in the respective cohorts, although this was not significant at enrolment (p=O.164). (iii) The immune complex binding capacities were found to strongly correlate with the level of expressions of complement regulatory protein, complement receptor type one on the erythrocytes, for cases and control, both during enrolment and follow-up. (iv) The erythrocyte immune complex binding interactions were significantly compromised when an anti-CRl specific antibody was used to block the CRl receptors on erythrocytes from children either with severe malarial anaemia, their symptomatic control or cerebral malaria and there symptomatic control. These findings suggest that there are differences existing between clinical groups with severe malaria and those with uncomplicated form of the disease. These differences may be relevant and pertinent to the pathogenesis and severity P. falciparum malaria.