The IL-4 deficiency was associated with impaired capacity to express IL-12 in the intestine early during infection, suggesting that this cytokine may promote dendritic cell activation [26]. Many studies with adult

mice have indicated that CD4+ T cells are crucial for establishing effective immunity against C. parvum or the gastric parasite C. muris [reviewed in ref. [8]]. A number of findings, however, cast uncertainty on a major protective function of T cells in the newborn mouse. For example, no increases in the percentages of CD4+ or CD8+ T cells in the Peyer’s patches or lamina propria were observed during infection [27, 28]. No antigen-specific activation of T cells was obtained in splenocytes taken from neonatal mice at different times during the patent infection period [29]. PFT�� solubility dmso In addition, β7−/− neonatal mice lacking the integrin α4β7 required for homing of activated mucosal T lymphocytes to the gut were shown to recover

from infection normally [30]. A recent report placed further doubt on the part played by CD4+ T cells or indeed, adaptive immunity in the control of C. parvum infection in neonates [28]. Repeated treatment of newborn mice with anti-CD4 neutralizing antibodies almost ablated the CD3+ CD4+ T cell population in the intestine and other lymphoid tissues but did not increase susceptibility to infection. In addition, similar acute patterns of infection were observed in neonatal C57BL/6 wild type and Rag2−/− mice. When adult wild type and Rag2−/− Masitinib (AB1010) mice previously infected as neonates were treated with an

immunosuppressive drug, however, relapse of infection was observed only in MAPK Inhibitor Library cell line Rag2−/− mice [28]. Even without treatment, relapse of infection that became fatal eventually occurred in most Rag2−/− mice. A similar effect was also observed in BALB/c SCID mice infected as neonates (Figure 1). These observations indicate that the innate immune response in neonatal mice is capable of bringing C. parvum infection under highly effective control. Also, although CD4+ T cells are required for ultimate elimination of the parasite they appear to play little if any part in the recovery from infection of murine neonates. This may not be entirely unexpected as there are few T cells in the intestine of newborn mice [31] and neonatal T cells may be poorly responsive against certain pathogenic organisms [32]. In addition, neonatal Th1 cells have a propensity to undergo apoptosis [33]. Neonatal hosts may compensate for an insufficiency in adaptive immune responses by having a heightened capacity to mount certain types of innate immune responses [34]. This may include enhanced ability to develop Toll-like receptor (TLR)-dependent inflammatory responses which could in part be due to reduced regulation of TLR activation pathways in neonates [35]. The role of TLRs in immunity to C. parvum is discussed below.