Blood samples collected from individuals belonging to an endemic area in Uttar Pradesh, were tested for plasmodial antigen specific immunoglobulin A (IgA) by enzyme immuno assay using soluble extract ofPlasmodium falciparum from culture. Among 773 (20.18%,P < 0.0001) samples 156 sera demonstrated a detectable seropositivity for antigen specific IgA. IgA levels were higher among individuals who experienced repeated attacks of malaria compared to acute infected patients. Among seropositive individuals the IgA titers were found increased with the age. Immunoglobulin isolated from sera having high level of IgA showed growth inhibitory effect inPlasmodium falciparum in vitro. A group of sera with high IgA antibody againstPlasmodium falciparum crude antigen showed seronegativity with specific peptides. Statistically, no positive or negative correlations were observed between antigen specific IgG and IgA. However, there was a tendency towards negative correlation between IgA and IgM. Mechanisms for the parasite specific IgA production remain to be established.

Culture supernatants of Concanavalin A activated human peripheral blood mononuclear cells were found to contain a factor which induced proliferative response in normal peripheral blood mononuclear cells. This proliferation-inducing factor specifically induced and sustained proliferation of purified human NK cells but not of T or B cells. Although interleukin 2 (IL12) also has proliferation-inducing effects on NK cells, the partially purified proliferationinducing factor preparations contained no measurable IL2 contamination. Moreover, neutralizing anti-IL2 antibodies did not block the growth effect of proliferation-inducing factor on purified human NK cells. Other cytokines which were tested, including IL4, IL6, IL7, IL12, TNF and IFN, were all found to be inactive in the proliferation-inducing factor assay. While proliferation-inducing factor by itself had no effect on T-cell proliferation, IL2-induced proliferation of T cells was significantly enhanced in the presence of proliferation-inducing factor, as was IL2-induced NK-cell proliferation. NK cells could be maintained in culture for at least a month in the presence of proliferation-inducing factor alone, but the cells lost their cytolytic activity after 3–4 weeks in culture. Addition of IL2, to NK cells which had been cultured in the presence of proliferation-inducing factor, restored their cytotoxicity. Proliferation-inducing factor activity was partially purified on an anion exchange HPLC column. The molecular weight of proliferation-inducing factor appeared to be about 10 kDa, based on its elution profile on a sizing HPLC column. Our results indicate that proliferation-inducing factor is a novel NK-cell proliferationinducing factor.