T cell receptor complementarity determining region 3 length analysis reveals the absence of a characteristic public T cell repertoire in neonatal tolerance. The response in the "tolerant" mouse within the residual repertoire is quantitatively similar but qualitatively different.

摘要: All adult BALB/c mice immunized with hen egg white lysozyme (HEL) or its dominant determinant, peptide (p)106–116, mount a T cell response using “public” Vβ8.2Jβ1.5 clone. Neonatal exposure to tolerance-inducing doses of antigen can drastically diminish responsiveness in the draining lymph nodes but not spleens animals challenged as adults cognate antigen. To determine role deletion anergy within mechanisms observed neonatal “tolerance,” we treated HEL and directly followed characteristic public clone complementarity determining region 3 length repertoire analysis. Our results confirm that despite intraperitoneal injection neonates high dose emulsified incomplete Freund's adjuvant, strong splenic proliferative was upon recall. However, these neonatally lacked usual HEL-primed mice. After challenge HEL–complete adjuvant adults, immunoglobulin (Ig)G2a isotype antibody reduced, IgG1 found be predominant anti-HEL IgG expressed, indicating deviation cytokine toward helper type 2. 5-wk-old mice, nasally instilled tolerogenic p106–116, also showed significant inhibition this expansion. These demonstrate during nasal tolerance induction, deletion/anergy removes clone, exposing similar specificity is characterized by 2 phenotype residence.