As TSLP has been shown to act on pulmonary macrophages directly to amplify their alternative activation state43,46, and as the TRM cluster expresses TSLP receptor (Crlf2), we also cannot rule out the possibility that TSLP functions in an autocrine manner and cooperates with IL-4 to maintain the M2-like phenotype of the dermal TRMs during infection. Here, IL4 is linked to infection.