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The mammalian immune system appears to play an essential role in preventing the development, and/or in controlling growth and spread, of malignant tumor cells. Antigenic properties of neoplastic cells and defense mechanism of the tumor host are briefly reviewed. The relative importance of immune reactions and other "non-specific" means of host defense with regard to tumor development and growth are discussed in the light of available experimental and clinical evidence. An attempt is made to incorporate these considerations into a hypothesis relating to the development of intestinal neoplasms.

Cytokinetic effects of 5 or 20 mg cyclophosphamide/kg body weight on thoracic duct lymph and blood cells of calves were analyzed. The larger dose caused a temporary cessation of lymphoid cell division, reduced the output of nondividing small lymphoid cells and impaired proliferation of neutrophil precursors. Feedback mechanisms acting on GO/G1 cells controlled the proliferation of lymphoid cells.

Recent work on the in-vitro analysis of granulocyte functions is reviewed. Various forms of granulocyte functions defect have been observed in association with increased susceptibility to infectious diseases. Intrinsic cellular defects can be distinguished from secondary impairment of granulocyte functions due to other diseases, iatrogenic causes or humoral defects. In such cases the in-vitro methods for evaluation of granulocyte functions have become an indispensable diagnostic aid.

This is a short overview concerning possible relationships between immunodeficiency and cancerogenesis/leukemogenesis. Following introductory remarks on concomitant and sinecomitant antitumor immunity, various factors/mechanisms that could influence tumor-host-interactions are discussed, in particular properties of neoplastic cell lines, the microenvironment, cellular components of nonspecific resistance, and specific, i.e. antigen-directed, cell-mediated and humoral immune responses against cancer cells. The increased incidence of malignant neoplastic processes in patients with inherited or acquired immunodeficiency raises the question if a lack of antitumoral defense or ineffective antiviral immunity is more important. Available data indicate that once a cancer has reached a certain size, the chances for the host to reject it solely with the help of its immune apparatus are minimal. The possibility remains that immune reactions may be more efficacious against small numbers of immunogenic tumor cells, i.e. in the very earliest phase of a neoplastic process and when the cancer begins to metastasize.

Renal manifestations of sarcoidosis are rare. In addition to calcium nephropathy, granulomatous interstitial nephritis and glomerulo-nephritis (GN) account for most cases. The latter two manifestations are described in 4 patients and in a detailed review of the literature. In comparison to a nonselected population of sarcoidosis patients, granulomatous interstitial nephritis is found more frequently in male patients above 40 years of age; it is associated more frequently with other extrathoracic manifestations of sarcoidosis; and it causes renal insufficiency of varying degree, which is at least partially reversible with steroid therapy. Predominant findings are silent microhematuria, sterile pyuria, mild proteinuria and a variety of tubular functional disorders. Glomerulonephritis (39 observations) has been described with increasing frequency in sarcoidosis. Because of the well known immunological abnormalities of sarcoidosis, frequent association of sarcoidosis with GN could be expected but this association has not yet been proven statistically. Sarcoidosis-associated GN includes a variety of histological forms, viz. membranous, proliferative and sclerosing GN. Glomerulonephritis may appear before sarcoidosis. Conversely, both diseases may appear simultaneously, or GN may follow all other manifestations of sarcoidosis with a latency period of many years.