CD4+ T cells play a key role in the immune response of pathogen-induced mastitis in dairy cattle. Mammary gland factor STAT5b is involved in the regulation of CD4+T cell differentiation during inflammatory response and milk production. Little is known about the genetic variation effects of bovine CD4 and STAT5b genes on somatic cell score (SCS) and milk production traits in dairy cattle. The aim of the study was to investigate the single nucleotide polymorphisms (SNPs) of bovine CD4 and STAT5b in Chinese Holsteins and to analyse their association with estimated breeding values (EBVs) for SCS and milk production traits. In the present study, SNPs of CD4 (NC_007303 g.13598C>T) and STAT5b (NC_007317 g.31562 T>C) were identified and genotyped in Chinese Holstein population. The results showed that both SNPs were significantly associated with the EBVs for milk yield and protein yield in Chinese Holstein cows, and the SNP in CD4 was associated with the EBV for SCS (P<0·01). The additive effect of CD4 SNP on protein yield was significant (P<0·05), and the dominant effect of STAT5b SNP was significant on milk yield and protein yield (P<0·01). Cows with combination genotype C7 (CCTT: CD4 g.13598C>T and STAT5b g.31562 T>C) had the highest SCS EBV but lower milk yield, while cows with C2 (TTTC) produced more milk, fat and protein than the other eight combination genotypes. These results suggested that the SNPs in CD4 and STAT5b may be potential genetic markers for SCS and milk/protein yields selecting and warrant further functional research.

In the present study, the expression of the CD4 molecule on murine egg plasma membrane was confirmed by the indirect immunofluorescence (IIF) method. The full-length CD4 cDNA from murine eggs was synthesised by the reverse transcriptase-polymerase chain reaction (RT-PCR) method and its authenticity verified by Southern blot hybridisation using an end-labelled internal oligonucleotide. The results of DNA sequencing showed that the nucleotide sequence of the cDNA of CD4 from murine egg mRNA was identical to that of immune T cells. To demonstrate the direct interaction of CD4 from murine egg with murine sperm cells bearing MHC (major histocompatibility complex) class II molecule, we employed a baculovirus expression system to generate CD4 on the surface of Spodoptera frugiperda (Sf9) cells. Expression of CD4 on Sf9 cells infected with autographa californica nuclear polyhedrosis virus (AcNPV)-CD4 was demonstrated by IIF and immunoblotting. The CD4-expressing Sf9 cells adhered to MHC class II-bearing sperm cells since the adhension was specifically blocked by anti-CD4 monoclonal antibody (mAb) or anti-monomorphic region of MHC class II mAb. Taking our previous and present experimental results together, they strongly suggest that intercellular membrane adhesion between two gametes at the fusion step in fertilisation is mediated by the MHC class II molecule located on the posterior region of the sperm head and the CD4 molecule on egg plasma membrane.

Although early reports on HIV and malaria in co-infected subjects indicated little apparent interaction between the two infections, more recent investigations have found evidence for HIV increasing the risk from malaria. Conversely, increased viral load in susceptible cells occurs in malaria-infected people. However, the overall pattern of results is still somewhat confusing and contradictory. While morbidity from malaria may be greater in HIV-positive patients and in several reports the mortality risk is also higher, major increases in blood-stage parasitaemias that one might expect are not generally observed. The results of surveys are summarized and discussed in the context of what is known of malaria and HIV immunology in the light of recent data from humans as well as animal models.

In recent years, interest in the use of computerized neuropsychological (NP) assessment measures has increased. However, there are limited data regarding how performance on these measures relates to performance on more traditional, clinical instruments. In the present study, 82 HIV+ men, who were all believed on clinical grounds to have neurobehavioral impairment, completed a traditional NP battery (TNB) and the California Computerized Assessment Package (CalCAP, a collection of computerized reaction time tests). Summary scores based on a TNB, as well as those based on the CalCAP, demonstrated significant associations with both degree of immunosuppression (CD4 count) and detectable viral load in cerebrospinal fluid, but not with detectable viral load in plasma. Established norms on the TNB and CalCAP batteries resulted in classifying 57% and 49% of the HIV+ sample as impaired, respectively. When using the TNB as the “gold standard,” impairment classifications based on CalCAP summary scores exhibited a sensitivity of 68% and a specificity of 77%. Overall agreement on impairment classifications between batteries was low (kappa = .44). Data from this study suggest that traditional NP batteries and computerized reaction time tests do not measure the same thing, and are not interchangeable in examining HIV-related NP impairments. (JINS, 2003, 9, 64–71.)

Resistance to the murine intestinal nematode Trichuris muris requires the development of a strong Th2 response. In a reconstituted SCID mouse model, CD4+ Th2 cells can mediate resistance to infection in the absence of antibody (Else & Grencis, 1996). The data presented here address the issue of how CD4+ T cells mediate this protective immunity within the SCID host. These studies demonstrate that timing and cell dose are critical if transfer is to result in resistance, with a minimum of 5 × 106 immune donor cells required to confer immunity. Furthermore, this CD4-mediated protective immunity only operates against the larval stages of the parasite. When the molecules necessary for activated CD4+ T cell migration to the GALT are inhibited with a cocktail of anti-integrin/addressin antibodies (anti-β7, anti-MAdCAM-1 and anti-αE), the resistance conferred by immune donor cells is completely abrogated. This implies that the effector mechanism acts locally at the level of the gut. CD4+ mediated cytotoxicity, directed against the epithelial cells inhabited by the parasite, could represent a novel, locally acting effector mechanism. However, Fas and Fas ligand-deficient mice, which are unable to mount CD4-mediated cytotoxic responses, readily expel T. muris indicating that the mechanism by which CD4+ T cells mediate protective immunity is unlikely to involve killing of infected gut epithelial cells.

The role of T-cells in development of experimental cerebral malaria was analysed in C57B1/6J and C57B1/10 mice infected with Plasmodium berghei K173 or Plasmodium berghei ANKA by treatment with anti-CD4 or anti-CD8 mAbs. Mice were protected against cerebral malaria (CM) when anti-CD4 or anti-CD8 mAbs were injected before or during infection. Even in mice in end-stage disease, i.e. with a body temperature below 35·5 °C, treatment with anti-CD4 or anti-CD8 antibodies or the combination protected against CM, whereas chloroquine treatment was completely ineffective in inhibiting further development of the cerebral syndrome.