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Fig. 1 | Retrovirology

Fig. 1

From: Clonal anergy of CD117+chB6+ B cell progenitors induced by avian leukosis virus subgroup J is associated with immunological tolerance

Fig. 1

Congenital infection of ALV-J caused abnormal development of immune organs and induced immunological tolerance. a Compared with the posthatch infection of chickens (n = 30) and mock infection of chickens (n = 30), ED6 infection of chickens (n = 30) was characterized by (1) poorly developed bursas of Fabricius, with bursal follicles with no differentiation into medulla (Me) and cortex (Co); (2) markedly decreased numbers of bursal follicles; and (3) hyperplastic interstitial connective tissue. b In chickens infected at ED 6 and infected at D 1, mild depletion of lymphocytes and multiplication of reticular cells were evident in the medulla. Tissue sections were stained by H&E (magnification: ×40, ×400). Arrows indicate the bursal follicles. c, d Quantitation of the degree of lesion. “++” indicates good development, “+”indicates dysplasia, “de” indicates depletion of lymphocytes, “de1” indicates mild depletion of lymphocytes, “de2” indicates severe depletion of lymphocytes. **p < 0.01, ***p < 0.001, two-way ANOVA was performed. e and f Compared with chickens infected at D 1 (n = 30), chickens (n = 30) infected at ED 6 showed severe immunological tolerance, which was characterized by the presence of high levels of ALV-J specific p27 antigen but the absence of detectable anti-ALV-J antibodies. Data are expressed as the mean ± SEM

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