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Drug induced immunosuppression of chicken immune response was studied in F1 hybrids of the CB and IC inbred lines. In tuberculin reaction complete inhibition of wattle swelling was induced by the administration of methotrexate, colcemid (1 mg/KBW), and 6-mercaptopurine. The cellular infiltration was substantially reduced in these cases. Cyclophosphamide and colcemid (0.1 mg/KBW) reduced partially the wattle swelling but had no apparent effect on the cellular infiltration. Acetinomycin D did not affect in measurable degree the wattle swelling. The histologic picture was in this case the same as in the control animals. The same drug administration schedule had less pronounced effect on anti-HSA antibody production. No anti-HSA antibody was found after the 500 mg/animal doses of 6-mercaptopurine. Significant reduction of anti-HSA titres was found after 50 mg/animal doses of 6-mercaptopurine, colcemid (1 mg/KBW), 25 MG/KBW or cyclophosphamide and after the methotrexate treatment.

Normal CBA mouse spleen cells were specifically depleted of cells spontaneously reacting to pigeon erythrocytes (PRBC) by two methods, the first allows specific depletion of anti-PRBC thymus derived (T) rosette forming cells (RFC) whereas the second depletes bone marrow derived (B) anti-PRBC hemolytic plaque forming cells (PFC). Depleted populations transferred into lethally irradiated syngeneic recipients and stimulated with PRBC failed to develop any significant response but they normally responded to a stimulation with sheep erythrocytes (SRBC). When spleen cells were taken from mice skin painted with picryl (trinitrophenyl: TNP) chloride 12 days before and the recipients were challenged in the same way and stimulated with PRBC, they become capable of producing a definite response to this antigen. Moreover in these animals, a consistent although low number of cells was found, which simultaneously reacted to both native PRBC and TNP conjugated SRBC. These findings show that unrelated delayed hypersensitivity reactions promote the immunological recovery of specifically depleted cell populations.

The potency of cytostatic and anti-inflammatory drugs was tested on the oxazolone-induced cutaneous basophil hypersensitivity (CBH) in mice. The challenge reaction was performed early after sensitization in order to minimize B-cell expression; exudative and cellular infiltration was estimated 6 h, 24 h and 48 h after challenge. The potency of drugs was tested at three different periods of immunization: 2 days before or after sensitization or before challenge. Cytostatics act mainly when cells are being committed, a corticoid acts on inflammation linked to committed cells, NSAIDs show inconstant anti-inflammatory effects on this test. D-Penicillamine and levamisole act in the same depressive profile in normal animals. Thus the CBH model appears to be relevant in studying drug activities on inflammation linked to T-cell expression.

Five non-steroidal anti-inflammatory drugs (indomethacin, naproxen, meclofenamic acid, feprazone and phenylbutazone: NSAIDs) and three glucocorticosteroids (dexamethasone, hydrocortisone and prednisolone) have been tested as local inhibitors of increased vascular permeability in guinea-pig skin. Lesions were induced by histamine or by antigen to evoke type I (passive cutaneous anaphylaxis), type III (reverse passive Arthus) and type IV (delayed hypersensitivity) allergic reactions. NSAIDs and glucocorticosteroids caused either weak, inconsistent inhibition or slight, high-dose inhibition of the response to histamine. None of the drugs tested showed significant inhibition of the type IV response. The NSAIDs caused dose-related inhibition of both type I and type III responses whereas glucocorticosteroids were ineffective. Maximum inhibition with the NSAIDs was never greater than 50--60% Feprazone, meclofenamic acid and indomethacin were the most potent inhibitors of histamine, PCA and Arthus responses respectively. The possible significance of the effects of these anti-inflammatory agents on vascular permeability is discussed.

Evidence is presented to indicate that there exists in lymphoid tissue, as a result of transforming lymphocytes, a new lymphokine which is chemotactically specific for lymphocytes, called 'lymphotactin'. Lymphotactin has been purified to electrophoretic homogeneity; has a molecular weight of 10,500 D and an isoelectric point of 5.9. Its role in amplifying the immune defense system by recruitment of naive lymphocytes into propinquity with the challenging antigens is suggested. Purification of macrophage migration inhibitory factor from thymus extracts to electrophoretic homogeneity leads to a compound of molecular weight of 36,500 D and an IEP of 6.9. Chemically it contains sialic acid and o-methyl glucopyranoside as its only carbohydrates. Purified MIF activates the macrophage phagocytically. Skin reactive factor and lymph node permeability factor have been isolated and purified and are found to be inhibited by pepstatin and antihistamine and to have an isoelectric point of pH 4.2 and a molecular weight of 50,000--100,000 D. It is believed that this anionic permeability increasing agent actually arises from the lysosomes of macrophages and lymphoblasts (the normal small lymphocyte having essentially no lysosomal organelles). The mononuclear cell infiltration characteristic of crude SRF and LNPF may proceed from their being contaminated with lymphotactin.

In vivo primed T cells injected into the footpad of naïve recipients elicit a typical delayed-type hypersensitivity (DTH) reaction in the presence of their specific antigen. Serial dilutions of primed T cell populations were used in order to score positive and negative transfers. The values for the footpad swelling obtained after these transfers followed a bimodal distribution. This clear bimodal distribution with no overlapping between positive and negative transfers suggested that a single cell initiates the DTH reaction. Limiting dilutions of cloned T cells transferred with their antigen allowed us to demonstrate that a single cell is able to transfer a specific DTH reaction.