While the depleted levels of IL-18 and IL-15 in the BAL of HTLV-1A/CoI-L infection favor a different mix of systemic pro-inflammatory and pro-resolution subsets, defined by elevated neutrophils producing IL-8 and CD11b alongside IL-10-producing non-classical monocytes, HTLV-1A/CoI-L infection again fails to recruit pro-resolution (IL-10) immune subsets to the lung at this late timepoint. The gene discussed is ITGAM; the disease is infection.