CD4 and infection: In contrast to the conventional understanding that ICs formed in chronic infections cause inflammatory response by FcγR cross‐linking, it was recently found that in mice with clone 13 LCMV (long term) infection, the presence of ICs resisted CD4+ T‐ and B‐cell depletion by anti‐CD4 and anti‐CD20 (rituximab) antibodies and blocked the activation of DCs by agonistic anti‐CD40.