These studies showed that a) ECM-resistance is independent of the immature myeloid hyperplasia (CD11b+/Ly6C+) characteristic of BXH2, as this trait is absent from resistant [BXH2×B6]F1 (Figure 6A), and b) is linked to brain infiltration of both myeloid (CD11b+/Ly6C+) and lymphoid cells (TCRβ+/CD4+ and TCRβ+/CD8+ T cells) in B6 mice (Figure 1E), and c) is concomitant with reduced production of IL12p40 by myeloid cells and impaired production of IFNγ by T cells following infection with P. berghei. The gene discussed is CD4; the disease is infection.