RoleofF4/80cells during induction ofhapten-specific contact hypersensitivity

SUMMARY F4/80, a monoclonal antibody thatbindstoa surface molecule on maturemacrophages and certain dendritic cells, hasbeenusedtoexplore theroleofepidermal anddermalcells asantigenpresenting cells (APC)during theinduction ofcontact hypersensitivity (CH)inmice.Systemic administration oftheantibody appeared tohavelittle or no physical or functional effect on intraepidermal Langerhans' cells, eventhough asubpopulation ofthese cells expressed theF4/80 ligand. Nonetheless, systemically administered F4/80antibodies were abletoimpair CH induction whendinitrofluorobenzene (DNFB)was painted on normalbodywallskinofBALB/c mice [anultraviolet B (UVB)-resistant strain]. Interestingly, systemic F4/80antibodies didnot affect CH induction inC57BL/10 mice(aUVB-susceptible strain). When a sensitizing doseof hapten was injected intracutaneously (i.c.) intoF4/80-treated BALB/candC57BL/10 mice, CH induction was impaired inbothinbred strains, although theseverity ofimpairment was greater in BALB/cmice.Following UVB radiation ofbodywallskin, anti-F4/80-treated BALB/cmice displayed veryfeeble CH,whether hapten was painted epicutaneously or injected i.c. atthe irradiated site. Based on these andother recentreported results, itisconcluded that(1)BALB/c micerelypartially upon dermal, F4/80+cells as a sourceofAPC whenhaptenisapplied epicutaneously, whereas C57BL/10 micerely almost exclusively upon epidermal Langerhans' cells inthis circumstance; and(2)after UVB radiation ofskin, BALB/cmicecan useF4/80+ dermal cells asthesourceofAPC function whenhapten is.painted epicutaneously. Thesefindings are discussed withrespect tothecellular basis forthedifferential susceptibilities ofgenetically defined strains ofmicetothedeleterious effects ofUVB radiation on CH induction.