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PubMed1975

Control of the immune response. I. Depression of DNA synthesis by immune lymph node cells.

The DNA response in the regional lymph nodes draining the site of immunization with contact sensitizing agents was assessed by measuring the uptake of radioactive iododeoxyuridine. The DNA response in the regional lymph nodes reached a peak on day 3 after immunization and fell to pre-immunization levels by day 6. The hypothesis was tested that lymph node cells from mice immunized with picryl chloride might depress the DNA response to the same antigen. Immune lymph node cells were injected intravenously and the recipient mice were immunized with picryl chloride on the same day. The immune cells depressed the DNA response on day 4 by an average of about 60 per cent. Smaller but significant depression also occurred on day 3. The cells responsible for the depression appeared in the regional lymph nodes 3-4 days after immunization and disappeared by day 21. The transfer of small numbers of immune cells (less than 2-5 X 10(6)) increased the DNA response in recipients 4 days after immunization with picryl chloride. The depression of the DNA response was largely specific. Pooled data from ten experiments showed that cells immunized with 4-ethoxymethylene-phenyl oxazolone ('oxazolone') caused no depression of the DNA response to picryl chloride, although in two of these experiments significant depression of about 21 per cent was seen. Similar results were obtained when immune cells were injected into mice immunized with 'oxazolone'.

Animals↗
PubMed1975

Bacteriocinogenic Clo DF13 minicells of Escherichia coli synthesize a protein that accounts for immunity to bacteriocin Clo DF16: action of the immunity protein in vivo and in vitro.

The Clo DF13 plasmid-specific immunity protein is able to prevent the inhibitory effect of cloacin DF13 on in vitro protein synthesis. We have shown, by gel filtration, that direct binding of the Clo DF13 immunity protein to cloacin occurs in vitro. This cloacin DF13-immunity protein complex is rather stable, and the cloacin present in the complex is no longer able to cause inhibition of in vitro protein synthesis. The binding of immunity protein to cloacin DF13 is rather specific because the Clo DF13 immunity protein does not bind to in vitro inactive cloacin and binds very poorly to the closely related bacteriocin colicin E3. Furthermore, we present data which strongly suggest that in vitro at least a fourfold excess of immunity protein is required to ensure that every cloacin molecule is inactivated by cloacin-immunity protein complex formation. Only a fraction (an about equimolar amount) of the immunity protein molecules, however, actually binds to cloacin DF13. The existence of an immunity protein-cloacin complex in vivo was concluded from the observation that cloacin, purified by chromatography on diethyl-(2-hydroxypropyl)-aminoethyl Sephadex in the absence of urea, contains an about equimolar amount of a second protein which comigrates with immunity protein on sodium dodecyl sulfate-polyacrylamide and urea-polyacrylamide gels. In an in vitro protein-synthesizing system, this component appeared to behave identical to the Clo DF13 immunity protein. The purified immunity protein-containing cloacin was at least 80 times less active in inhibiting in vitro protein synthesis, compared to cloacin, free of immunity protein. These data imply that few, if any, cloacin DF13 molecules are present in cloacinogenic cells as active, free cloacin molecules.

Bacterial Proteins↗
PubMed1977

Adoptive transfer of immunity from mice immunized with ribosomes or live yeast cells of Histoplasma capsulatum.

This investigation was designed to compare the role of lymphoid cells and immune serum in protective immunity induced by immunization with ribosomes or live yeast cells of Histoplasma capsulatum. Spleen cells, peritoneal cells, and serum from C3H mice immunized with Histoplasma ribosomes or live cells were transferred intravenously to separate groups of syngeneic recipients. All recipients along with a set of immunized and control mice were challenged intravenously with 4 x 10(6) yeast cells of H. capsulatum, and protection was assessed. Immunization with ribosomes or live cells provided 90 to 100% protection. Mice receiving filtered spleen cells or peritoneal cells from donors immunnized with live cells showed 90 to 100% protection; 80 to 90% protection was observed for mice receiving cells from ribosome-immunized donors. In contrast, no evidence of protection was seen in mice receiving serum from either live-cell- or ribosome-immunized mice. Peritoneal cells were far more efficient than spleen cells in adoptive transfer of immunity. The adoptive immunity in recipients persisted for at least 3 weeks after transfer, the longest period tested in the present study. These results indicate that the immunity elicited by immunization with Histoplasma ribosomes or live cells is mediated by a cellular mechanism.

Animals↗
PubMed1978

Experimental immune pancreatitis in the mouse by rabbit immune sera directed against purified enzymes of the exocrine pancreas.

An experimental xenogeneic immune pancreatitis was induced in AB-mice by repeated intraperitoneal injections of rabbit immune sera directed against purified pancreatic enzymes (alpha-amylase, lipase, trypsin) for 3 hours up to 8 days. Histologically, the immune pancreatitis is characterized by three different findings: 1. Multiple acinar cell necroses on the 2nd, 3rd and 5th day of immune serum application. 2. A dedifferentiating acinar cell atrophy with development of pseudocanalicular acini on the 5th and 9th day. 3. An increasing interstitial histiolymphoplasmocytic pancreatitis on the 5th and 9th experimental day. Ultrastructurally, the acinar cell necroses proved as the final stage of a step-by-step developing acute lethal cell damage. The dedifferentiating acinar cell atrophy corresponds to a chronic sublethal cell injury with alteration of different cytoplasmic components. The interstitial pancreatitis in immune serum treatment is characterized by differently activated histiocytes and lymphocytes as well as by mature plasma cells. Because of immune histological findings (peri- and intraacinar deposition of rabbit globulin, specific fixation of guinea-pig complement, and appearance of mouse globulin in the mouse exocrine pancreas) and control experiments with rabbit and mouse normal serum as well as with physiological saline, the pathogenesis of the induced xenogeneic immune pancreatitis is regarded as a twophase process: 1. The acinar cell necroses are mainly due to a cytotoxic immune reaction (possibly in combination with an immune complex reaction) caused by specific anti-pancreatic enzyme antibodies of the applied immune sera. The dedifferentiating acinar cell atrophy may be the result of a specific action of the anti-enzyme antibodies against the corresponding pancreatic enzymes in the apical secretion granules of the pancreatic acinar cells. 2. The interstitial histiolymphoplasmocytic pancreatitis is mainly the morphologic substrate of an extravascularly (intraperitoneally) induced serum sickness reaction (immune complex reaction) due to the foreign proteins applied with the xenogeneic immune sera.

Amylases↗
PubMed1976

Mediation of immune responses to tumor antigens in vitro by immune RNA.

It was shown that normal nonimmune C3H mouse spleen cells became specifically cytotoxic to chemically-induced syngeneic C3H tumor cells by incubation with xenogeneic I-RNA extracted from the lymphoid organs of specifically immunized guinea pigs. This response was specific for the tumor used to immunize the I-RNA donor. In a totally syngeneic system, we showed that syngeneic I-RNA extracted from the spleens of tumor-bearing rats mediated cytotoxic immune reactions which were directed specifically against the tumor-associated antigens of syngeneic rat tumor target cells. Active antitumor I-RNA synthesis in the lymphoid organs of I-RNA donor animals reached a maximum between days 14 and 21, depending on the route of administration and the nature of the immunizing tumor. Active I-RNA preparations were insensitive to treatment with deoxyribonuclease or pronase, but were inactivated by ribonuclease treatment; thereby indicating that the active moiety was one or more species of RNA. The active fractions of the I-RNA preparations had sedimentation values in sucrose density gradients of 12-16S, and comprised only a small fraction of the total RNA present in the lymphoid cells. Active antitumor I-RNA appeared to be localized in the cytoplasm of sensitized lymphoid cells, rather than in the nucleus. Lymphocytes from normal human donors as well as from cancer patients, when incubated with xenogeneic or allogeneic I-RNA, became specifically cytotoxic for human tumor cells in vitro. Crossreactivity among tumors of the same histologic type was observed, but not crossreactivity with tumors of other histologic types. Xenogeneic I-RNA extracted from the lymphoid organs of donor animals immunized either iwth tumor cells or normal tissues, following incubation with normal allogeneic lymphocytes, mediated cytotoxic immune reactions which were directed both against tumor-associated antigens and normal transplantation antigens. However, when autologous lymphocytes were used as effector cells, only immune reactions directed against tumor-associated antigens were observed. Allogeneic I-RNA extracted from peripheral blood lymphocytes of human cancer patients mediated specific cytotoxic immune reactions that were directed against common tumor-associated antigens shared by human tumors of similar histologic type. I-RNA's directed against "self" normal cell surface antigens appear to be recognized as self by lymphocytes, and immune responses against these self antigens are not elicited. On the other hand, I-RNA's directed against "nonself" tumor-associated antigens induce lymphocytes to effect specific antitumor immune responses. Our data are consistent with the hypothesis that I-RNA is an information-containing ribonucleic acid molecule capable of mediating immune reactions in vitro which are specific for the tumor-associated antigens of the tumor used to immunize the I-RNA donor.

Animals↗
PubMed1992

Do knowledge and attitudes about influenza and its immunization affect the likelihood of obtaining immunization?

A telephone survey was conducted on 190 patients in Barcelona, Spain, at high-risk for influenza to evaluate the relationship between their knowledge and attitudes toward influenza and influenza immunization and whether they received the immunization. A discriminant function correlates (r = 0.86) with the immunization behavior and predicts the behavior before flu immunization in 84% of cases if we know the previous immunization behavior and adequately classifies the behavior in 82% if we don't know it (r = 0.75). Modifiable factors that predict immunization are self-identification as high-risk, belief that the immunization will not cause discomfort, intention to be immunized, and physician assigned. Those not immunized had a prevalent feeling that the shot is not effective, that they are not susceptible to the illness, and that the health center does not offer satisfactory organization to provide immunization. Furthermore, they felt that they had received controversial information through the mass media. We therefore believe that health education activities regarding influenza immunization should be specifically directed to increasing awareness of those who belong to a high-risk group, as well as to emphasizing susceptibility to the illness and the innocuousness of the immunization.

Aged↗
PubMed1975

Antitoxic immunity in experimental cholera: protection, and serum and local antibody responses in rabbits after enteral and parenteral immunization.

The protective effect of enternal and parenteral immunization with cholera toxin antigen against experimental cholera in rabbits was studied by using the small-bowel loop technique. Subcutaneous injection of crude toxin as well as purified toxin or toxoids gave rise to significant protection against toxin challenge. The enhanced resistance to toxin was found to correspond to a many-fold higher magnitude of protection against challenge with live vibrios. In the primary response the protection increased during the first month. Booster immunization gave rise to a further increased immunity which, however, declined rapidly. Multiple oral or repeated intraintestinal antigen administrations also induced protective antitoxic immunity although of less magnitude than that obtained by parenteral immunization. Enteral and, to a lesser extent, parenteral immunization gave rise to increased antitoxic antibody titers and immunoglobulin levels in intestinal washings and mucosa scraping. Immunoglobulin G (IgG) and IgG antitoxins predominated, but after enteral immunization total IgA and specific IgA antibodies occasionally reached levels similar to those for IgG. In serum, significantly increased antibody levels (IgG) were only recorded after parenteral immunization. Both the primary binding and the neutralizing antitoxin titers showed a stayistically significant correlation with the degree of protection against toxin challenge; however, for the neutralizing antibodies this correlation was not without exceptions. No relation to protection was found for intestinal antibodies. The results of the present study indicate that enternal as well as parenteral immunization with toxin antigen can give rise to effective cholera immunity. After enternal immunization, the protection appears to be medicated by locally synthesized antibodies. After parenteral vaccination both serum-derived and locally produced antibodies seem to be effective.

Administration, Oral↗
PubMed1977

Induction and expression of immunity after BCG immunization.

The induction and expression of immunity to Mycobacterium tuberculosis after BCG immunization by intravenous, subcutaneous, and pulmonary routes has been investigated in mice. The speed with which protective immunity was engendered was a function of inoculum size; the immunization route was a less influential factor. Tuberculin hypersensitivity varied both with the inoculim size and immunization route, being least after pulmonary immunization. Once immunity was established, a steady state ensued in which the number of sensitized lymphocytes in the spleen was similar, regardless of the route or dose of vaccination. Actively immunized animals controlled intravenous and subcutaneous challenge infections, regardless of the method of vaccination. However, pulmonary challenge was resisted most efficiently by mice immunized by the pulmonary route. Adoptive immunity was well expressed in the spleen only, but the lungs were no more deficient in this regard than the footpad. It is suggested that enhanced immunity in the lungs depends on a population of resident sensitized lymphocytes.

Animals↗
PubMed1978

Protective antitoxic cholera immunity in mice: influence of route and number of immunizations and mode of action of protective antibodies.

An adult mouse model has been elaborated for studies of experimental cholera (Vibrio cholerae enterotoxin-induced intestinal secretion) and protective antitoxic immunity in either ligated small bowel loops or intact small intestine. Mice of different inbred strains varied markedly in intestinal susceptibility to toxin, C57B1 being the most sensitive strain tested. Fluid accumulation started within 1 h after the inoculation of toxin and was maximal after 5 h, whereafter recovery gradually ensued. The dose-response curve was sigmoid, the ED50 of crude toxin being equivalent to about 0.1 microgram purified toxin/cm in the loops and 0.3 microgram/cm in the nonligated intestine. Two peroral (p.o.) immunizations induced significant protective immunity which increased markedly after two further immunizations by the same route. Additional p.o. immunizations did not appreciably enhance the protective immunity any further. Intravenous (i.v.) vaccination had to be repeated more than 5 times before intestinal immunity could be observed. No correlation between serum antitoxin titers and protective immunity was found. Electron microscopic examination revealed that whereas peroxidase-coupled cholera toxin bound tightly to intestinal microvilli from unimmunized or 5-times i.v. immunized mice it did not bind to the microvilli of p.o. immunized animals. The data thus suggest that the protective immunity is mediated exclusively by locally produced antibodies which prevent the binding to toxin to the gut epithelium.

Administration, Oral↗
PubMed1975

Duration of circulating and secretory antibody and cell-mediated immunity following immunization.

An important consideration in evaluating vaccines is the duration of immunity. The only really important measure of this immunity is the protection against infections and/or illness at various time intervals, following natural or artificial challenge. There are few data of this sort, more commonly immunity is estimated by measuring serum antibody, in many instances an erroneous measure. Serum antibody levels to respiratory viruses fall only slightly 6 months following infection or immunization. It is difficult to assess the duration of antibody for much longer than this, because of problems with intercurrent infection. With respiratory bacterial infections, e.g. pneumococcal pneumonia, parenterally-induced immunity probably lasts for only several months. Secretory antibody induced by inactivated viral vaccines, seems to persist for about a year, after having reached a peak level at about 4-6 weeks following immunization. Work with the live attenuated polio virus vaccine indicates longer lasting immunity, with detectable antibody persisting for up to 34 months. Restimulation with the inactivated polio virus vaccine produced no evidence of a secondary response (memory). Following booster immunization with influenza very little evidence of memory is seen. Cell-mediated immunity (CMI): in guinea pigs BCG sensitization can be demonstrated for at least 2-9 months. In humans, intracutaneous BCG immunization leads to positive tuberculin reaction in 6-10 weeks, and skin sensitivity lasts an average of about 4 years. There is contradicting data as to the duration of protection against infection following BCG immunization. Local and systemic CMI have been shown to exist independently of each other in experimental animals and man.

Animals↗
PubMed1979

Dissociation of anti-tumor immune responses in rats immunized with solubilized tumor-associated antigens from a methylcholanthrene-induced fibrosarcoma.

Soluble tumor antigens were prepared from chemically-induced rat fibrosarcoma KMT-17 cells by various methods [Na-deoxycholate (DOC), 3 M-KCI extraction, and crude membrane preparations by mechanical disruption]. Soluble tumor antigens prepared by DOC extraction (DOC-STA) could be detected by a radioisotopic footpad assay (FPA) and they showed the strongest antigenic activity in KMT-17 immune rats. Anti-tumor immune responses in rats previously immunized with DOC-STA were measured by FPA, Winn assay, and transplantation resistance. Significant responses detected by the FPA and Winn assay were demonstrated in rats immunized with DOC-STA. However, rats previously immunized with DOC-STA showed a significant enhancement of tumor growth when challenged with KMT-17 cells. This enhancement was specific for the tumor line used. Normal rats which received adoptive transfer of thymus and spleen cells from rats immunized with DOC-STA produced specific enhancement of tumor growth as compared with non-treated rats. Administration of cyclophosphamide before immunization with DOC-STA abrogated the enhanced tumor growth in the host. These results suggest that immunization with soluble tumor antigens specifically enhanced tumor grwoth by the induction of immunosuppressor cells. Dissociation between the anti-tumor immunity detected by the FPA and Winn assay and the enhanced tumor growth detected by transplantation resistance in rats immunized with DOC-STA is discussed.

Animals↗
PubMed1976

Immune processes in the course of infection with dysentery bacilli. II. Transfer of immunity by means of serum.

The role of antibodies in immunity to intravenous infection with dysentery bacilli was studied in mice. Serum from animals immunized with a single dose of live dysentery bacilli obtained at a varying intervals of time after immunization transferred immunity to other mice infected with lethal doses of the same bacilli. Passive immunity transferred with serum was diffrentiated. Sera obtained 4 to 8 days after immunization of the donors with sublethal doses of live Shigella sonnei phase I bacilli protected lethally infected recipients by inhibiting multiplication of the bacilli in the spleen and liver. Highest protective activity of this type was found in sera obtained 6 days after immunization of the donors. Sera obtained after 11 days and later protected the recipients from death, but only negligibly inhibited growth of the bacilli in the internal organs of the animals. It is suggested that immunity to intravenous infection with dysentery bacilli in mice follows a biphasic course. In the first phase, between days 4 and 8 after immunization, cell-mediated immunity and a specific humoral factor play the main role. In the second phase, specific immunoglobulins of the IgG class afford protection.

Animals↗
PubMed1979

Tumor-specific immunity induced by somatic hybrids. II. Elicitation of enhanced immunity against the parent plasmacytoma.

Hybrid cells derived from fusion of a BALB/c plasmacytoma (TEPC-15) and L cells (C3H origin) were used to stimulate tumor-specific immunity against the parental plasmacytoma cells. Live hybrid cells induced tumor-specific immunity against TEPC-15 more effectively than mitomycin-treated hybrid or TEPC-15 tumor cells. Adoptive transfer of immunity with spleen cells of mice immunized with hybrid cells was also more effective than that with mitomycin-treated tumor cells. The immunity induced by the hybrid cells was specific to the TEPC-15 tumor because the mice that received immune spleen cells were not protected against challenge with either HOPC-8 or McPC-603 plasmacytomas. T cell populations were primarily responsible for the transfer of specific immunity based on the sensitivity of immune cells to anti-Thy 1.2 and complement. Mice that had established solid tumors were treated with 5 x 10(7) spleen cells to evaluate the therapeutic value of the hybrid-induced immune cells. Tumors in the mice that received immune cells gradually regressed over a 40-day period, whereas tumors on the control mice continued to grow. These results suggest that a rearrangement of tumor-specific antigens on allogeneic hybrid cells can enhance their immunogenicity.

Animals↗