Analysis of neonatal T cell and antigen presenting cell functions.

Neonates are more susceptible to infection than adults and exhibit more intense or prolonged clinical symptoms. The extent to which deficiencies in T cell or antigen presenting cell (APC) function underlie hyporesponsiveness is incompletely understood. Here, immune function of cord blood mononuclear cells (CBMC), from healthy, full-term neonates was compared with adult PBMC. As widely reported, polyclonally-stimulated T cell proliferation was found to be equivalent, while IFN gamma responses were markedly lower amongst neonates. Reasoning that such stimuli may elicit responses qualitatively different from those that would be obtained following MHC-dependent, cognate T cell activation, alloantigen-specific responses were evaluated. Strikingly, neonates exhibited IFN gamma, IL-4 and IL-10 production equal to adults in short term primary culture. Both the frequency (Fisher's p < 0.0004) and intensity (< 7.5 vs 36.5 pg/ml; Wilcoxon P = 0.005) of alloantigen stimulated IL-5 responses were elevated among neonates, a finding equally evident using irradiated adult or neonatal cells as stimulators. Finally, the relative capacity of neonatal APC as stimulators of cytokine synthesis was assessed by a novel approach using CBMC as both responders and stimulators in MLR. Irradiated neonatal cells consistently stimulated similar proliferative but substantially lower IFN gamma responses than did adult APC, independent of responder origin. The data argue; (i) T cells are largely immunocompetent at birth, (ii) accessory cell function is not fully mature, and (iii) the widely observed hyporesponsiveness to pathogenes may be primarily due to immaturity of APC function or costimulator molecule expression.

Arbitrary single short primers identify polymorphic DNA markers that distinguish inbred strains of mice.

The inbred mouse strains, Balb/c and SJL/J, have been widely used in biomedical research to unravel the genetic basis of susceptibility to tumors, viral diseases, autoimmune encephalitis, atopic disorders and neuro-retinopathies. In this study we attempted to identify DNA polymorphisms that distinguish them using RAPD assay. Screening of the genomic DNA of mice with a panel of 100 random decamer primers led to the identification of 36 primers which amplified 204 strain specific RAPD markers. On an average each of the selected primer amplified 11 bands of which 5.6 were strain specific. Segregation of RAPD markers in a (Balb/c x SJL/J) F1 x SJL/J backcross progeny (n = 6) suggested that the markers are potentially suitable for molecular genetic linkage studies.