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Antimelanoma antibodies previously demonstrated in the serum of melanoma patients by immunofluorescence have now been detected by a sensitive and quantitative complement fixation technique. The melanoma-specific antibodies detected by both of these techniques show a remarkable correlation with the stage of disease. Study of serums from 63 melanoma patients showed that both the incidence and titer of antibodies to the tumor antigens of malignant melanoma were found to be higher in patients with localized melanoma than in those with widespread metastatic disease. Furthermore, study of serial serum specimens on melanoma patients revealed a drop in antibody titer to undetectable levels with advancing metastatic disease. Additional evidence for the importance of immunological factors in this disease came from studies of delayed cutaneous hypersensitivity in melanoma patients. All patients with localized melanoma were capable of being sensitized to DNCB, whereas all patients who could not manifest delayed cutaneous hypersensitivity to this chemical had widespread metastatic disease. Eight melanoma patients were treated with immunotherapy using BCG as an immunological adjuvant. This therapy produced a rising titer of antimelanoma antibody and temporary tumor regression in five patients. However, only one of these patients has had a complete regression and remains free of disease at two years following treatment. There was a good correlation between the patient's immunological competence and his response to immunotherapy. All patients who could be sensitized to DNCB or tuberculin and developed a fourfold rise in antibody titer had some response to immunotherapy, whereas anergic patients failed to respond to this therapy. These studies indicate that the host immune response to malignant melanoma is an important factor in controlling the progression of this disease. Therefore, immunotherapy may become a useful adjunct to the primary surgical therapy of malignant melanoma.
Immunopathophysiological mechanisms in endometriosis-associated reproductive failure were studied in appropriate populations: infertile and fertile women with and without endometriosis. The incidence of sera positive for any of the autoantibodies tested among infertile women with endometriosis (n = 25) was similar to that observed in the three control groups [unexplained infertility patients (n = 25) and fertile women with (n = 10) and without (n = 25) endometriosis]. The mean volume of peritoneal fluid was significantly elevated in women with endometriosis (both fertile and infertile) as compared with patients without endometriosis (fertile or infertile). The concentration of peritoneal fluid leukocytes and the percentage of cells positive for macrophage markers were significantly increased and the percentage of T lymphocytes significantly decreased in infertile women with endometriosis but not in patients with unexplained infertility and fertile women with endometriosis, as compared with fertile controls without endometriosis. Macrophages from infertile patients with endometriosis had higher sperm phagocytosis than did those from infertile women without endometriosis or fertile subjects with or without endometriosis. Incidences of serum and peritoneal fluid samples embryotoxic to the in-vitro development of 2-cell mouse embryos were significantly higher in infertile patients with endometriosis than in unexplained infertility patients and fertile women with or without endometriosis. It is concluded that immunological mechanisms of endometriosis-associated infertility exist but that these peritoneal immunological factors in infertile women with endometriosis are related to their subfertility rather than to the presence of ectopic endometrial implants. This is supported by the lack of immunological abnormalities observed among fertile women with endometriosis. These immunological abnormalities are lacking in patients with unexplained infertility.
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The majority of strokes (85-90%) result from cerebral ischemia. In most cases extra - and intracranial vessel atherosclerotic changes are considered to be responsible for cerebral ischemia. A sudden failure of cerebral circulation is usually combined with instability of atherosclerotic plaques. Pathologic studies demonstrate that atherosclerosis simultaneously involves the whole arterial vessel tree. The mechanism of atherosclerotic plaque formation is similar in different regions of the arterial system, including the brain supplying arteries. The essence of atherosclerosis appears to be an excessive inflammatory-fibroproliferative response to various forms of the arterial wall injury. The development of unstable plaques is closely related to the inflammatory process involving the arterial wall. Immunological factors seem to play an important role in the development of atherosclerotic changes and their destabilization. Imaging techniques for arteries supplying the brain are known. None of them gives a clear answer about plaque instability. Taking into account the role of the inflammatory process in the pathogenesis and instability of atherosclerotic changes, measurement of serologic markers of plaque instability seems to be complementary to imaging methods for diagnosis of unstable atherosclerotic plaques. The inflammatory aspect of atherosclerosis should be reflected in the prophylaxis of the central nervous system vascular disorders.
This review summarizes data on the cross-reactions observed among the subtypes of Streptococcus pneumoniae. Types 6A and 6B; 19F, 19A, 19B, and 19C; 18F, 18A, 18B, and 18C; and 23F, 23A, and 23B were examined with use of radioimmunoassay for measurement of inhibition of binding; the cross-reactions are discussed in terms of the known chemical structures of the antigens involved. Cross-reactions observed with use of rabbit antisera proved to be an unreliable guide to the responses observed thus far in humans. Cross-reactions of pneumococcal capsular polysaccharide antigens with other bacterial antigens are mentioned. These cross-reactions are analyzed with the idea of maximizing the effectiveness of the pneumococcal vaccine. Immunologic factors that may determine the quality and/or quantity of the immune response to immunization are discussed. These factors include antigenic competition and influence of preimmunization levels of antibody. Antigenic competition, although not a major concern with the present vaccine, may determine the upper limit of the number of capsular types that can be present in a single vaccine. The preimmunization level of antibody may determine the specificity of the antibody produced after vaccination.
PROBLEM: More than 90% of human immunodeficiency virus type 1 (HIV-1) infection in children is acquired by mother-to-child transmission. However, infection of the child occurs in between 14 and 35% of cases. METHOD OF STUDY: To understand the mechanisms involved in HIV-1 transmission, we have investigated the antigenic, molecular, and phenotypic characteristics of the virus harbored in infected mothers and their children. RESULTS: A clear correlation was observed between the transmission of the virus and the isolation of viral variants with a rapidly replicating and syncytium-inducing phenotype from the mother. Furthermore, non-transmitting mothers were able to neutralize several primary isolates more frequently than transmitting mothers. The comparison of the viral phenotype and genotype of mother-child pairs showed that the transmitted virus did not have common features, suggesting that transmission is usually not a selective process. CONCLUSIONS: This study suggests that transmission is governed by an interaction of both viral and immunological factors. The results obtained indicate that different strategies can be applied for the prevention of transmission.
Direct Coombs' antiglobulin tests were performed on 80 dogs with patent Dirofilaria immitis infection and 170 dogs negative for microfilaria of D. immitis. Presence or absence of anemia was determined by hematocrit in 55 of the heartworm negative dogs and 68 of the dogs with heartworm disease. Heartworm infected dogs showed a higher incidence (37%) of anemia than noninfected dogs (14.5%). Anemia was most prevalent in two groups of dogs with heartworm infection, one group showing vena caval syndrome (91%) and the other occult dirofilariasis (62.5%). These latter two groups of dogs also showed a significantly higher number of positive Coombs' reactions at 37 degrees C than other dogs with heartworm disease and the noninfected dogs. The number of positive Coombs' reactions at 4 degrees C among the total of 80 dogs with heartworm infection was significantly higher than that for dogs without heartworm disease. However, there was no positive correlation between anemia and the outcome of the Coombs' test at either temperature. These findings do not suggest that immunologic factors play a major role in the pathogenesis of anemia in dogs with heartworm disease.
Platelet subendothelium interaction is an essential step in thrombosis and hemostasis which can be modulated by immunoglobulins, immune complexes, complement, and leukocytes. Antiplatelet antibodies can induce thrombocytopenia which is accompanied by a reduced vascular wall thickness and an increased fenestration. Antigen-antibody complexes can activate platelets inducing platelet release and aggregation. This reaction is amplified by the first component of complement C1q. Cytotoxic antibodies directed against endothelial cells have been observed in transplantation. These antibodies can be directed against HL-A antigens or specific endothelial antigens. Anticollagen antibodies have been detected in patients with leprosy. The C1q component can inhibit adhesion of platelets to collagen and platelet aggregation induced by collagen. The association of acquired or congenital C1q deficiency and vasculitis has been reported. C3a is taken up by endothelial cells and metabolized. C3a and C5a can modify vessel wall permeability and activate granulocytes which can become toxic for endothelial cells. Leukocyte cationic protein can reduce platelet aggregation. An anti-von Willebrand antibody could be the origin of hemostatic abnormalities and endothelial lesions. The involvement of immunologic factors in platelet vessel wall interactions is complex. Immune complexes and some antibodies seem capable of promoting thrombosis, while a component of complement (C1q) may also have an antithrombotic role.
Optimal and early control of recent onset, type I diabetes by intensive insulin therapy has been reported to allow insulin withdrawal in about two thirds of subjects treated. We used continuous s.c. insulin infusion (CSII) in the attempt to induce a temporary remission of insulin dependence in 18 newly diagnosed young adult diabetics. After 10 days of optimized glycometabolic control, insulin infusion was stopped and patients were switched to glibenclamide (15 mg/die) plus metformin (1 g/die). Diabetics were considered in remission of insulin dependence when their metabolic control fulfilled the following criteria for at least 3 months: absence of glycosuria, pre- and post-prandial blood glucose less than or equal to 120 and 180 mg/dl, respectively, HbA1c less than or equal to 7%. Insulin therapy could be discontinued for periods of over three months in 11 subjects (61%) and for as long as 18 months in one case. Insulin requirement during CSII was slightly higher in nonremitters (NR) than in remitters (R): 0.36-0.64 vs 0.26-0.41 U/kg/die. After 24 months from CSII, R still showed lower insulin requirement (0.35-0.42 U/kg/die) than NR (0.55-0.75 U/kg/die). Further, the role of some hormonal and immunologic factors was investigated. Plasma C-peptide and glucagon were measured, fasting and 2h after each meal, both on admission and immediately after CSII, when patients were switched to oral therapy. No difference in hormone levels could be detected on admission, whereas, after CSII, mean post-prandial increase of C-peptide over basal was significantly higher in R than in NR (1.18 +/- 0.37 vs 0.22 +/- 0.16 ng/ml, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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OBJECTIVE: Although it is well documented that breast milk provides optimal nutrition and immune benefits to the infant, factors that influence the immunologic composition of breast milk are less understood. A recent study reported that immunoglobulin A (IgA) levels in breast milk are lower after exercise compared with resting concentrations. However, the women exercised until exhaustion. The effect of moderate exercise on immunologic components in breast milk has not been reported. Therefore, the purpose of this study was to 1) compare the levels of immunologic compounds in breast milk of exercising women with the milk of sedentary women and 2) determine whether 30 minutes of moderate exercise affects immunologic properties of breast milk. METHODS: Exclusively lactating women were studied at 3 months' postpartum. Women in the exercise group (EG; n = 29) reported exercising aerobically at least 30 minutes/d for 3 days/wk, and women in the sedentary group (SG; n = 24) had exercised once a week or less during the previous 6 weeks. Cardiovascular fitness levels and concentrations of IgA, lactoferrin, and lysozyme in milk were measured. A subsample of the EG (n = 17) participated in a 30-minute exercise session at 75% of maximum heart rate and a rest session of 30 minutes of sitting rest on 2 separate days. Breast milk samples were collected before and 10 and 60 minutes after exercise and rest sessions. IgA, lactoferrin, and lysozyme concentrations were measured. RESULTS: Women in the EG had a higher level of cardiovascular fitness than women in the SG (39.7 +/- 1.0 vs 32.4 +/- 1.0 mL O(2)/kg/min). Milk concentrations of IgA, lactoferrin, or lysozyme were not significantly different between groups. In addition, there were no significant differences in the concentrations of IgA, lactoferrin, or lysozyme after moderate exercise compared with sitting rest. CONCLUSION: Moderate exercise during lactation improves cardiovascular fitness without affecting levels of IgA, lactoferrin, or lysozyme in breast milk.
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Comprehensive clinical and immunologic studies carried out in 38 patients with neurochorioretinitis have demonstrated the contribution of infection to the etiology and pathogenesis of this condition and helped identify the nature, mostly infectious, of the condition in 55.3% of patients. Toxoplasma infection, revealed in 39.5% of cases, is one of the major etiologic factors of neurochorioretinitis. Tuberculous etiology of the condition is more rare (7.9% of cases). The autoimmune systemic component was detected in 7.9% of the examinees. Immunopathologic shifts, presenting as hyperimmunoglobulinemia, were fairly frequent (71.9% of patients), excessive concentrations of circulating immune complexes were detected in 78.6% and cryoglobulins were found in 42.9% of the examinees, this permitting the authors to regard neurochorioretinitis as a form of immunocomplex conditions of the eye, most possibly, of an infectious origin. Blood group A (II) was found to be a risk factor for neurochorioretinitis patients; according to the literature data, this is explained by a reduction of the interferonogenic activity. Etiotropic anti-inflammatory drugs, including corticosteroids, and interferon preparations for the risk group patients appear to be advisable for the therapy of neurochorioretinitis.
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