IFNG and infection: Taking our above findings showing that both IFNγ and TNFα are required as in vivo mediators of bone loss, that IFNγ likely acts through indirect mechanisms and that soluble factors produced by infected macrophages induce osteoclast production, we hypothesize that IFNγ may act on macrophages during infection to potentiate TNFα production, which in turn directly or indirectly promotes osteoclast activity.