This paper describes the trapping of antigen in lymphoid follicles of rat popliteal lymph nodes as revealed by electron microscopic radioautographs following injection of 125I-labeled Salmonella adelaide flagella and other materials. The antigen was taken up vigorously, and to an approximately equal extent, by both primary and secondary follicles. The rate of uptake was faster in preimmunized than in virgin adult rats. The bulk of the antigen in follicles was extracellular, and persisted in this location for at least 3 wk. Label was most frequently found at or near the surface of fine cell processes. Many of these were branches of dendritic follicular reticular cells. Such processes interdigitated with equally fine processes of lymphocytes, creating an elaborate meshwork. In some cases, antigen was found between lymphocytes which appeared to be in close apposition. Occasionally, a few grains appeared over lymphocyte nuclei and study of serial sections suggested that this probably represented true entry of small amounts of antigen into lymphocytes. The characteristic "tingible body" macrophages (TBM) of germinal centers appeared to play only a secondary role in follicular antigen retention. They showed degrees of labeling over their phagocytic inclusions varying from negligible to moderately heavy. Moreover, follicles lacking or poor in TBM retained antigen just as effectively as those containing numerous TBM. The hypothesis is advanced that TBM may be derived from monocytes that migrate down from the circular sinus. Follicular localization of three other materials was also studied, though not in such detail. These were 125I-HSA complexed to anti-HSA: 125I-labeled autologous IgG; and 125I-monomeric flagellin. All of these showed the basic features of intercellular, membrane-associated deposition noted with 125I-flagella. The role of follicular antigen depots in immune induction is discussed. The tentative conclusion is reached that follicular antigen in a primary follicle encounters natural antibody on the surface of certain antigen-reactive lymphocytes. The resultant reaction causes blast cell transformation and eventually the genesis of a germinal center.
SUMMARYMycoplasma mycoides var. mycoides requires for growth a number of preformed lipid precursors. Media containing glycerol, cholesterol, a saturated and an unsaturated fatty acid, defatted bovine serum albumin and an additional defatted serum protein fraction (Fraction C) can supply these requirements. Albumin is believed to function by binding fatty acids, and Fraction C by binding cholesterol. The requirement for a saturated fatty acid can be satisfied by myristic, palmitic, stearic or margaric acid, lauric acid being less effective. The requirement for an unsaturated fatty acid can be satisfied by oleic acid, linoleic and linolenic acids being less effective. Organisms incubated in a medium deficient in either glycerol, the Fraction C +cholesterol system, or oleate, but adequate with respect to all other nutrients, died rapidly. Death was accompanied by lysis. Death due to a deficiency of glycerol or of cholesterol was prevented either by the omission of uracil (an essential nutrient) or by addition of chloramphenicol. Death due to oleate deficiency was not prevented by the omission of uracil. Morphological changes which resulted from each of these deficiencies are illustrated by electron micrographs. The hypothesis is advanced that glycerol, cholesterol and long-chain fatty acids are all needed for the synthesis of an undetermined cell component which is necessary for the structural integrity of the cell, and that the synthesis of this is more sensitive to a deficiency of these nutrients than is the synthesis of cytoplasm.
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