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The numbers of mast cells and of eosinophil granulocytes in the mouse uterus have been counted under various conditions. The mast cells increased in number during pregnancy and the elevated level persisted for at least three months. They also increased, though less, during the aging of the virgin animal. In unilateral pregnancy, mast cells of the non-pregnant side increased in number as compared to a virgin uterus. In four-parous, spayed mice 17β-oestradiol brought about no change in the number of granulated or degranulated mast cells. Eosinophil granulocytes began to increase in number only when the uterus had become fully oedematous. It is concluded that the eosinophilotaxy of the uterus is brought about by the oestrogen although not via a degranulation of the uterine mast cells.

Human respiratory mast cells, which were obtained coincidentally with diagnostic bronchial brush biopsy, were maintained under conditions for short-term tissue culture. Most mast cells were viable and degranulated on exposure to antibody to immunoglobulin E or to the mast cell degranulating agent compound 48-80. The degranulation of human mast cells is characteristically an intracellular process with no extracellular extrusion of granules.

It is suggested that mast cells and basophil leucocytes, or some subpopulation of such cells, are post-mitotic derivatives of thymus-derived lymphocytes. The evidence would be strengthened if the present controversy about Ig receptors on T cells should be resolved in favour of the alternative: that the receptors are passively derived from monomeric IgM produced by B cells and thus analogous to the passively obtained IgE receptors of mast cells.

NUMEROUS experimental investigations have revealed the importance of mast cells for allergic reactions. Symptoms of anaphylactic shock result from the liberation of biologically active substances by mast cells. However, the way in which mast cells are affected by antigen-antibody reactions is still not understood.

EARLIER investigations have shown that incubation of isolated rat peritoneal mast cells with purified anti-rat IgG-globulin and fresh serum in vitro results in a cytotoxic immune reaction1. Data demonstrating that this process is inhibited by various agents, especially by alkyl phosphates and synthetic chymotrypsin substrates, indicate that the activation of a chymotrypsin-like esterase is of some importance for the reaction2. The enzyme, which is contained in the heat labile serum portion, shows many striking similarities to an enzyme of the complement complex (C′1-esterase), and was therefore thought to be identical with it3. Further experiments, however, revealed that neither a euglobulin preparation with high C′1-esterase activity nor purified human (C′1a-esterase, irrespective of whether or not antibody is also present, produces detectable morphological or pharmacological changes in isolated rat mast cells (ref. 3 and Lepow, I. H., personal communication). The question thus arose as to what extent the immunological behaviour of mast cells would be influenced by pre-treatment with various enzymes. The data presented here provide some insight into the problem.

The present study was undertaken to determine if human IgE immunoglobulin could be shown to bind to rat peritoneal mast cells and to establish whether binding is a prerequisite for the cellular alterations taking place during the rat mast cell test. It was found that sensitization of rat mast cells occurs very rapidly in the presence of human IgE immunoglobulin. Thus, incubation of the IgE immunoglobulin at 37°C for 3 min with rat mast cell suspension and washing the suspension once with medium 199 led to morphological changes in the mast cells on challenge with anti-human IgE immunoglobulin. However, attempts to correlate longer periods of incubation time with increased sensitization or show the extent of binding by multiple washings of the cell suspension were unsuccessful due to the lability of the rat mast cells. On the other hand, significant uptake of IgE immunoglobulin was observed by the mast cells after exposing the cell suspension to (a) radiolabelled 125I-IgE immunoglobulin for 3 min at 37°C an...