Analysis of T helper and antigen-presenting cell functions in cord blood and peripheral blood leukocytes from healthy children of different ages.

Abstract

The development of antigen-specific functional T lymphocyte immunity in infants and children is an area of immunology that needs elucidation. Leukocytes from cord blood (CBL) and from PBL of children of different ages who were in the hospital for minor surgical procedures were compared with PBL from healthy adults for their ability to generate T helper cell (Th) responses assessed by in vitro proliferation and IL-2 production after stimulation with: influenza A virus (FLU); tetanus toxoid (TET); adult allogeneic PBL that were either undepleted (ALLO) or depleted ofadherent antigen presenting cells (ALLONW); and PHA. CBL generated Th responses to AL-LONW, ALLO, and PHA, but not to FLU or TET. PBL from infants between 6 and 13 mo of age responded to ALLO and PHA; none responded to FLU or ALLONW, and two of four responded weakly to TET. PBL from children between 13 and 26 mo ofage responded to all stimuli except FLU, to which only one child responded marginally. PBL from children older than 36 mo responded to all stimuli at levels comparable to those of PBL from adults.The use of undepleted and adherent cell-depleted CBL and PBL from children of different ages as allogeneic stimulators of responses generated by PBL from adults indicated that the antigen presenting function of CBL and PBL from children 13 mo or older are sufficiently developed to present alloantigen, whereas PBL from children younger than 13 mo are not. Therefore, our results indicate that age-dependent differences exist in both T helper and antigen-presenting functions of CBL and PBL from children of different ages. Surprisingly, CBL appear to be more efficient in antigen-presenting function than PBL from children younger than 13 mo. These findings are important for establishing developmental parameters of T helper cell immunity relevant for pediatric infection and transplantation in infants and children. (J. Clin. Invest. 1993. 91:2829-2836

Retrovirally Mediated IFN-β Transduction of Macrophages Induces Resistance to HIV, Correlated with Up-Regulation of RANTES Production and Down-Regulation of C-C Chemokine Receptor-5 Expression

“…5 Type I IFN are known to increase the frequency of Th1 cells (39 -42). During the progression of AIDS, there is a decreased expression of Th1-type cytokines concomitant with an increased expression of Th2-type cytokines, resulting in altered immune responses (43,44). Our results show that IFN-␤ transduction of macrophages can favor the development of a Th1-type immune response that would be beneficial in HIV-infected patients because it restores Th1-type immune responses.…”

Adult Javanese migrants to Indonesian Papua at high risk of severe disease caused by malaria

“…These differences may be strictly developmental [16,17] or established by exposure to non-P. falciparum antigens experienced through the normal course of life [18]. Intrinsic age-related changes to the immune system may be the basis of profoundly distinct immune responses to repeated infection by P. falciparum, and thus significantly affect the clinical course and consequence of infection.…”

Characterisation of CTL directed towards non-inherited maternal alloantigens in human cord blood

“…10,17,18 CBMC immaturity and prevalence of suppressor functions are consequences of poor antigenic experience 10 and foetalmaternal immunological interactions, 18 which operate to prevent both foetal rejection and GVHR towards maternal tissues during pregnancy. The absence of immunological memory determines the incapacity of CBMC to be activated in vitro by recall antigens, 19 but, apparently, does not impair the ability of these lymphocytes to proliferate and secrete lymphokines in response to allogeneic stimuli. [20][21][22] Even though alloantigen priming of cord blood T lymphocytes can induce a strong proliferative response, it has been demonstrated that this initial activation leads to a state of unresponsiveness of cord blood T lymphocytes when re-challenged with the same alloantigens.…”