Kawasaki disease affects infants and children, leading to inflammatory changes of blood vessels which is often accompanied by fever and lymph node swelling. Patients also develop inflammation of cardiac tissues and valves, and, in some cases, aneurysms or thrombi are formed. The causes of KD are unknown, although the onset of the disease appears related to infection as supported by epidemiological observations of endemic KD .
There is an indication that children with KD are characterized with expansion of peripheral blood B cells with CD180-positive phenotype, compared to control samples . Notably, patients with viral infections similarly exhibit upregulated proportions of CD180-positive B cells, although to a lesser degree, further indicating a link between viral infection and KD. From the limited number of observations, the importance of CD180 expression on expanding population of B cell was unclear.
It is known that B cells are activated in KD, producing antibodies, perhaps in response to viral or bacterial infection. Given the preferential expression of CD180 by memory B cells and the involvement of CD180 in B cell activation and immunoglobulin production, it is possible that CD180 plays a role in the development and pathophysiology of KD. CD180-overexpressing B cells in KD could therefore represent a subset of activated B cells.
Differences in CD180 might also modulate the function of other receptors in B cells in KD. For example, given the known functional interactions with classical members of the TLR family, CD180 could modulate TLR function which could, in turn, lead to the production of pro-inflammatory cytokines and perpetuation of the KD phenotype.
Recently, SARS-CoV-19 infection has been implicated as an etiological factor in the initiation of KD or a KD-like syndrome. Observational studies indicate significant increases in Kawasaki-like disease in areas with high prevalence of SARS-CoV-19 infection, suggesting a role for the novel Corona virus in the presentation of KD (Verdoni et al.