Changes with time in Langerhans cell number, ATPase reactivity and morphology in murine epidermis after exposure to UVB.

Effects on Langerhans cells of a single 200 mJ/cm2 dose of 284-316 nm UVB were studied in the dorsal epidermis of CBA/H mice. ATPase-positive cells were counted using light microscopy and compared with numbers of cells containing Birbeck granules. In interfollicular epidermis from untreated mice 633 +/- 20 (mean +/- S.E., n = 30) ATPase-positive cells/mm2 were found. By 3 days after UVB treatment, the number of ATPase-positive cells decreased by 90%, whilst the Birbeck granule-containing cell population was only reduced by 40% and very few cells had ultrastructural damage, suggesting that many Langerhans cells lost ATPase marker but remained intact. 7 d after irradiation there were 50% more cells with Birbeck granules than in controls, but the number of cells bearing ATPase remained below normal. ATPase-positive cell numbers approached normal only after a further 2-3 weeks. Langerhans cell responses after UVB differed from those previously found after X-irradiation.

Comparative studies on B cell reactivities in two X-linked immunodeficient mice to the B cell-stimulating factors.

Responsiveness of B cells from X-linked immunodeficient CBA/N and DBA/2Ha mice to the B cell growth factor-1 (BCGF-I or BSF-1) and B cell differentiation factors (B151-TRF1 and B151-TRF2) was comparatively studied. B cells from CBA/N mice did not respond to BSF-1 in the presence of soluble anti-mu antibody. However, the BSF-1-response of CBA/N B cells was detected when activated by the anti-mu antibody-coupled Sepharose-beads. In the B151-TRF1 assay, antigen-unprimed B cells from CBA/N mice failed to respond to B151-TRF1, whereas antigen-primed B cells became responsive to B151-TRF1. In the B151-TRF2 assay, CBA/N B cells were non-responder to B151-TRF2. In these assays, however, unprimed CBA/N B cells were able to absorb both B151-TRF1- and B151-TRF2-activities to the same extent as the non-defective strain B cells. These results indicate that B cell defect in CBA/N mice may be reflected by some abnormality in signal transmission at encounter to the B cell-stimulating factors but not by inability to bind these factors. These low responder properties of CBA/N B cells were all inherited in an X-linked recessive manner. In contrast, B cells from DBA/2Ha mice well responded to BSF-1 and B151-TRF2, whereas both antigen-unprimed and -primed DBA/2Ha B cells failed to respond to B151-TRF1. This selective B151-TRF1-unresponsiveness of DBA/2Ha B cells was also controlled by an X-linked recessive inheritance. Moreover, in contrast to CBA/N mice, selective unresponsiveness of B cells to B151-TRF1 in DBA/2Ha mice was reflected by the absence of B151-TRF1-receptor expression, as demonstrated by absorption experiment. The B cell populations found in these two distinct X-linked immunodeficient mice may provide an useful experimental model for analyzing B cell activation process mediated by various B cell stimulation factors.