Macrophages malignant cells

It is also more or less accepted that T-cells, in particular T-helper cells (CD4+), may develop into either Thl cells or Th2 cells. By doing so, T-helper cells orchestrate the ensuing immune response by the types of cytokines they produce. Thl cells, by producing IL-12 and y-IFN, stimulate macrophages and/or cytotoxic T-cells to kill and destroy infected or malignant cells, or to initiate a delayed type hypersensitivity (DTH) reaction Th2 cells, by producing IL-4, IL-5, IL-10, IL-13, trigger B-cells to initiate antibody production. 

Localized cntaneous lesions were sometimes noted after snbcntaneons injection and mimicked those described with GM-CSF. Injection-site subcutaneous nodules infiltrated by lenkemic cells have been found in patients treated for acnte leukemia (SEDA-19, 343), but in two other patients, inflammatory macrophages were misinterpreted as malignant cells (SEDA-20, 337). 

The macrophage-derived tumor necrosis factor level in plasma is elevated in thrombotic conditions associated with malignancy (93). Likewise, mast cell-derived platelet-activating factor levels in plasma are increased in thrombotic conditions accompanied by mast cell activation (93). 

Cyclosporine reduces production of cytokines involved in T-cell activation and has direct effects on B cells, macrophages, bone, and cartilage cells. Its onset appears to be 1 to 3 months. Important toxicities at doses of 1 to 10 mg/kg/day include hypertension, hyperglycemia, nephrotoxicity, tremor, GI intolerance, hirsutism, and gingival hyperplasia. Cyclosporine should be reserved for patients refractory to or intolerant of other DMARDs. It should be avoided in patients with current or past malignancy, uncontrolled hypertension, renal dysfunction, immunodeficiency, low white blood cell or platelet counts, or elevated Ever function tests. 

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