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64 prepuberal gilts in 4 groups were treated with 400 PMS + 200 HCG (Suigonan - Vemie) (I), 100 FSH + 100 HCG) (II), 200 FSH + 200 HCG (III) ("international units") or served as untreated controls (IV). One halve of the groups laparotomized at the 12th day p.i. had ovulated 100, 25, 75 and 12,5% resp., the other halve slaughtered at the 36th day p.i. had ovulated to 83, 43, 88 and 50% resp. Sexual cycle was registered in 50, 29, 43 and 12.5% of the animals. Zystic ovaries (greater than or equal to 11 mm) developed only in a few cases in I and III.
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Some moderate and extreme thermophilic bacteria grew well on media other than the recommended basic media. Attempts to induce phenylalanine hydroxylase (Phe H) in the various thermophiles as well as mild thermophily in the mesophiles Pseudomonas sp ATCC 11299a and Chromobacterium violaceum ATCC 12540 were unsuccessful. Evidence is presented indicating that the enzyme in the latter two organisms may be membrane bound. The level of Phe H activity induced was not always consistent with the level of the inducer phenylalanine (Phe) in the growth medium.
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By the aid of two alkylating agents (cyclophosphamide (CP) and 036.5122, (Asta), applied after a single dose of antigen, tolerance to sheep red blood cells (SRBC), has been induced in NMRI mice. Duration and characteristics of recovery were followed by a second antigenic challenge at various time intervals and by determination of 19 S and 7 S plaque-forming cells (PFC) 4 days later. During recovery from the tolerant state two phases of responsiveness could be differentiated: an early phase with no or markedly reduced numbers of total PFC, all of them being of the IgM type; a later phase with a steady increase in total PFC up to normal values, paralleled by an increase in the proportion of 7 S PFC finally reaching 90% of total PFC. In comparison with CP, recovery from tolerance induced by equitoxic doses of 5122 were delayed and modified. Even after 8 weeks, total PFC to SRBC were still depressed, and the ratio 19 S/7 S PFC resembled neither a typical primary nor secondary pattern. It is concluded that CP-mediated immunological tolerance is followed spontaneously by the establishment of a memory state. This observation, in agreement with findings of other authors, is interpreted as the expression of an established B cell memory compartment during the period of deficient T cell activity. The long-lasting modification of specific responsiveness after 5122 indicates a profound disturbance of the potency to recover from the impact of this alkylating agent, the biological base of which is as yet unidentified. It is suggested that observation of the characteristic features during the recovery phase from tolerance may help to clarify the nature of the defect in specific responsiveness.
Injection of a single dose of cyclophosphamide (CY) (125 mg/kg) or a combination of a small dose of CY (20 mg/kg) and 2.5 mg/kg lipopolysaccharide induces a transient appearance of autoreactive T lymphocytes (T-ARC) in the spleens of mice. The T-ARC activity reaches a peak 6 days after CY injection and could not be detected 8 days after this treatment. For testing T-ARC activity, spleen cells were injected into the footpads of syngeneic recipients, and the resulting lymph node enlargement at the draining site of cell inoculation and the content of nucleated cells in the lymph node was determined. Possible explanations of this autoimmune phenomenon are discussed. It is postulated that CY-resistant precursors of T-ARC are stimulated by "new" antigenic sites present on the surface of B lymphoblasts repopulating the CY-damaged spleen in a period of transient absence of CY-sensitive suppressor cells.
Co-stimulation through CD28 is thought to be necessary for the activation of unprimed CD4+ T cells, which are otherwise rendered tolerant. However, we previously found that CD4+ T cell priming was normal or augmented in mice which overexpressed a soluble form of CTLA4 where co-stimulation through CD28 was abrogated. To investigate this CD4+ T cell response, we exploited the capacity of the superantigen staphylococcal enterotoxin B to stimulate T lymphocytes bearing V beta 8+, which represent approximately 30% of all CD4+ T cells. In litter-mate controls of CTLA4-Ig transgenic mice, immunization with staphylococcal enterotoxin B leads to expansion, followed by deletion of V beta 8+ T cells, and the remaining cells are tolerant when stimulated in vitro. Comparable expansion and deletion of V beta 8 T cells occurs in CTLA4-Ig transgenic mice. However, in contrast to normal mice, the remaining V beta 8+ T cells from CTLA4-Ig transgenic mice are not anergic and remain responsive to superantigen in vitro.