Why does the autoantibody against cytokine incease in patients with idiopathic pulmonary alveolar proteinosis?

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Recent studies have revealed that neutrophils from PAP patients had reduced basal functions such as phagocytosis, cell-adhesion, H_2O_2 production, and microbial killing (Uchida, et. Al.. NEJM.2007). In contrast, we found that some subsets of peripheral blood T and B cells were activated or excessively matured compared to normal controls. In CD4^+ cells, the number of naive T cells was reduced and the effecter-memory/naive ratio was up-regulated. Interestingly, small amount of CD4^+ cells were proliferating ex vivo without any stimulation. In B cells, CD38^+ activated cells were increased in both naive and memory B cell subset, whereas the expression of CD19 was reduced compared to the controls. Cells expressing CD138, a plasma cell marker, were significantly increased. Importantly, GM-CSF autoantibody was detected in the culture supernatants of peripheral blood mononuclear cells after 2 days incubation without any stimulation. These results suggested that some subsets of T and B cells were driven to be matured/activated and possibly promoted to produce the autoantibody.