Apparent Difference in the Roles of Spleen and Lymph Nodes in the Pathogenesis of Host-Versus- Graft Disease in Murine Parent/F1 Chimeras

Immunodeficiency in RFM/(T6xRFM)F1 mouse chimaeras with lethal host-versus-graft syndrome

“…2). As was the case with donor cells capable of proliferation or of antibody production [20], donor T lymphocytes were present in greater numbers in HVG nodes than spleens (Table 3). Because the percentages of F) donor T lymphocytes in host spleens and nodes remained relatively constant, it is apparent that there were increases in their total numbers as those organs increased in size and cellularity.…”

“…It is also possible that some B cells were activated by LPS, but could not proliferate because of decreased synthesis of B cell growth and maturation factors. Late in lethal HVG disease there are marked decreases in thymic-dependent antibody responses [8], and declines in serum IgGl levels [14] and in the percentages of mature F) donor antibody-forming cells [20] that may signal a waning of T cell help and decreased output of IL-6 [25]. In pilot studies, IL-4 was not detected in cultures of splenic or nodal cells from 21-day-old HVG mice.…”

“…The background proliferation observed was almost surely initiated by the HVG reaction, and therefore should not be considered spontaneous. It involves diverse types of haematopoietic and lymphoid cells [6], and cells from both host and graft [20]. High background counts and poor Con A responses are also seen in mice which develop non-lethal disease after the perinatal inoculation of F, cells with both class I and II differences [3].…”

“…The stable colonization of donor T (Table 3) and B cells [13], and the increases in percentages of replicating F] cells [20] in RFM host spleens and nodes would usually be accepted as signs of tolerance. However, the sustained hyperplasia of host and donor cells (Table 1) and the allogeneic effect on F| donor B cells [13] indicated that full tolerance was not achieved.…”