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At least 19 recordsLinked to original sources

PubMed1984

Immunity to Babesia in mice. I. Adoptive transfer of immunity to Babesia rodhaini with immune spleen cells and the effect of irradiation on the protection of immune mice.

Immunisation of Balb/c mice against Babesia rodhaini by an amicarbalide-controlled infection resulted in a solid immunity which lasted for 216 days. With spleen cells of immune mice protection could be transferred both to naive mice pretreated with cyclophosphamide. Treatment of naive mice with cyclophosphamide (300 mg/kg) five days before a lethal B. rodhaini inoculation resulted in over 50% survival. This protective effect of cyclophosphamide is explained by its inhibiting effect on suppressor T-cells. The protection against B. rodhaini challenge infection afforded to immune Balb/c mice was completely resistant to a sublethal irradiation of 400 rad. Since B-lymphocyte function in antibody production is suppressed by this dose, the role of antibodies in the effector phase of the immunity appears to be of minor if any importance. A considerable degree of protection was still preserved after irradiation of immune animals with 875 rad. Sensitivity to this irradiation dose of all immunocompetent cells except macrophages and a small fraction of T-lymphocytes indicates the involvement of these cell types in the effector phase of the specific immunity. Highly radioresistant macrophages are therefore considered to play the major role but T-lymphocytes are also required for complete protection.

Animals↗

PubMed1980

Cell participation in immune response by immune ribonucleic acid. I. The role of T lymphocytes in immune response by immune RNA against T-dependent antigens.

T- and B-cell participation in the immune response induced by immune ribonucleic acid (iRNA) preparations against T-dependent antigens was studied using athymic nude, neonatally thymectomized (NT) and cyclophosphamide-treated (CY) mice. The iRNA(T + B) preparations were made from the spleen of BALB/c mice immunized with these antigens. Injection of the iRNA into nude or NT mice caused an increase in the number of specific rosette-forming cells (RFC) and of memory cells capable of responding to secondary stimulus with a small dose of the corresponding antigen. Injection with T-dependent antigens or with iRNA(T + B) did not cause any immune response in CY mice, suggesting depletion of the B-cell function. The iRNA(T) and iRNA(B) were prepared, respectively, from the thymuses of BALB/c mice and from the spleens of nude mice which had been immunized with T-dependent antigens. Injection of nude mice with both iRNA(T) and iRNA(B) caused an increase in the number of specific RFC and the secondary antibody formation response after boosting with a small dose of the corresponding antigen. Injection of iRNA(T) preparation into nude mice could induce the anamnestic response after boosting. However, neither of the iRNA(T) or iRNA(B) preparation could induce in nude mice the proliferation of the number of specific RFC. These results indicate the presence of at least two kinds of iRNA preparations against T-dependent antigens and that the cooperation of iRNA(T) and iRNA(B) was required for the induction of immune response against T-dependent antigens.

Animals↗

PubMed1982

Specific cross-immunity between Trichinella spiralis and Trichuris muris: immunization with heterologous infections and antigens and transfer of immunity with heterologous immune mesenteric lymph node cells.

Infections with either 300 infective Trichinella spiralis larvae or 400 embryonated eggs of Trichuris muris were infective in eliciting accelerated expulsion of heterologous challenge infections given 20 days after the primary infection. Accelerated expulsion could also be achieved by the administration of soluble crude worm antigen given 12 days prior to heterologous challenge or by adoptive transfer of mesenteric lymph node cells taken from mice infected with the heterologous parasite. Each species is capable of eliciting an accelerated secondary expulsion response in hosts that have been actively or adoptively immunized against the other species and these results are taken to indicate that there is a specific cross-immunity between T. spiralis and T. muris due to shared antigens. It is postulated that these shared antigens are derived from stichocyte granules.

Animals↗

PubMed1992

Immunization with extracellular proteins of Mycobacterium tuberculosis induces cell-mediated immune responses and substantial protective immunity in a guinea pig model of pulmonary tuberculosis.

We have studied the capacity of a selected fraction of Mycobacterium tuberculosis extracellular proteins (EP) released into broth culture by mid-logarithmic-growth-phase organisms to induce cell-mediated immune responses and protective immunity in a guinea pig model of pulmonary tuberculosis. Guinea pigs infected with M. tuberculosis by aerosol but not uninfected control guinea pigs exhibit strong cell-mediated immune responses to EP, manifest by dose-dependent cutaneous delayed-type hypersensitivity and splenic lymphocyte proliferation. Guinea pigs immunized subcutaneously with EP but not sham-immunized control guinea pigs also develop strong cell-mediated immune responses to EP, manifest by dose-dependent cutaneous delayed-type hypersensitivity and splenic lymphocyte proliferation. EP is nonlethal and nontoxic to guinea pigs upon subcutaneous immunization. Guinea pigs immunized with EP and then challenged with aerosolized M. tuberculosis exhibit protective immunity. In five independent experiments, EP-immunized guinea pigs were consistently protected against clinical illness, including weight loss. Compared with EP-immunized guinea pigs, sham-immunized control guinea pigs lost 12.9 +/- 2.0% (mean +/- SE) of their total weight. EP-immunized guinea pigs also had a 10-fold reduction in viable M. tuberculosis bacilli in their lungs and spleens (P = 0.004 and 0.001, respectively) compared with sham-immunized control animals. In the two experiments in which some guinea pigs died after aerosol challenge, EP-immunized animals were protected from death. Whereas all 12 (100%) EP-immunized guinea pigs survived challenge with aerosolized M. tuberculosis, only 6 of 12 (50%) sham-immunized control guinea pigs survived challenge (P = 0.007, Fisher exact test). This study demonstrates that actively growing M. tuberculosis cells release immunoprotective molecules extracellularly, that a subunit vaccine against tuberculosis is feasible, and that extracellular molecules of M. tuberculosis are potential candidates for a subunit vaccine.

Aerosols↗

PubMed1986

Cells involved in the immune response. XXXII. Surgical extirpation of the spleen in the early memory period following primary i.v. immunization of the outbred rabbit results in a marked impairment of a subsequent immune response to the specific antigen: an immunological explanation for the overwhelming postsplenectomy syndrome.

Rabbits immunized intravenously(iv) with sheep erythrocytes(SRBC) (primary response) pass through a period which begins at about Day 35 postprimary immunization and extends to about Day 120 during which time all detectable spontaneous AFC (immediate PFC) and memory AFC(cells which generate PFC in culture) are detected only in the spleen. Prior to Day 30 postprimary iv immunization, large numbers of immediate PFC are detected in the circulation and the bone marrow as well as in the spleen. By Day 120 postprimary iv immunization, memory cells can be detected in significant numbers in the thymus and the popliteal lymph nodes (PLN) as well as in the spleen. The number of memory cells in the PLN and thymus increases over the course of the following 6 months. Rabbits splenectomized on Day 40 postprimary iv immunization and subjected to reimmunization iv with 10(9) SRBC 1, 5, or 8 months later were unable to give significant secondary immune responses. Only the thymus and PLN cells, cultured in vitro with the antigen(SRBC), 1, 5, or 8 months postprimary immunization, generated secondary immune(PFC) responses and these responses were feeble at best. The failure of the immunized rabbit to give a significant secondary immune response to SRBC if splenectomy was first carried out at a time postprimary iv immunization when all memory cells to the original antigen are sequestered only in the spleen (i.e., days 40 to 100) constitutes an animal model which provides a credible immunological explanation for the postsplenectomy syndrome which affects a minority of splenectomized individuals. These individuals, like the rabbits splenectomized on Day 40 postprimary immunization, lack the capacity to evoke a strong secondary immune response to particular infectious microorganisms and succumb in a few days with fulminant septicemia unless aggressive chemotherapy is instituted upon initial sign of infection.

Animals↗

PubMed1998

Differences in immune responses induced by oral and rectal immunizations with Salmonella typhi Ty21a: evidence for compartmentalization within the common mucosal immune system in humans.

Based on the concept of the common mucosal immune system, immunization at various inductive sites can induce an immune response at other, remote mucosal surfaces. The immune responses elicited through rectal and oral routes of antigen delivery were compared with respect to (i) measurement of antibody responses in serum and various external secretions of the vaccinees and (ii) characterization of the nature and homing potentials of circulating antibody-secreting cells (ASC). Specific ASC appeared in the circulation in 4 of 5 volunteers after oral and 9 of 11 volunteers after rectal immunization with Salmonella typhi Ty21a. The kinetics, magnitude, and immunoglobulin isotype distribution of the ASC responses were similar in the two groups. In both groups, almost all ASC (99 or 95% after oral or rectal immunization, respectively) expressed alpha4 beta7, the gut homing receptor (HR), whereas L-selectin, the peripheral lymph node HR, was expressed only on 22 or 38% of ASC, respectively. Oral immunization elicited a more pronounced immune response in saliva and vaginal secretion, while rectal immunization was more potent in inducing a response in nasal secretion, rectum, and tears. No major differences were found in the abilities of the two immunization routes to induce a response in serum or intestinal secretion. Thus, the rectal antigen delivery should be considered as an alternative to the oral immunization route. The different immune response profiles found in various secretions after oral versus rectal antigen administration provide evidence for a compartmentalization within the common mucosal immune system in humans.

Administration, Oral↗

PubMed1992

Transmission immunity in malaria: reflections on the underlying immune mechanisms during natural infections and following artificial immunization.

Malaria transmission-blocking immunity has been studied in natural malarial infections in man, during infections in animals and following artificial immunization of animals with sexual stage malaria parasites. Effective immunity, which prevents infectivity of a malarial infection to mosquitoes, has been observed under all of these circumstances. Two general types of effector mechanism have been identified. One is an antibody mediated mechanism which acts against the extracellular sexual stages of the parasite within the midgut of a blood feeding mosquito. The other is a cytokine mediated mechanism which inactivates the gametocytes of the parasites while still in the circulation of the vertebrate host. Both effects have been observed during natural infections and following artificial immunization. The basis of induction of transmission-blocking immunity, including the nature of the memory for such immunity, however, may be very different in different host/parasite systems and during natural infection or following artificial immunization. Following artificial immunization a strong immune memory for transmission blocking immunity has been observed in animal systems. By contrast, following natural infections in man immune memory for transmission blocking immunity has been found to be weak and short lived if it occurs at all. It is suggested that the immunogens which induce natural transmission blocking immunity may be CD4+ independent.

Animals↗

PubMed1993

Comparison of humoral immune responses and tumor immunity in mice immunized with recombinant SV40 large tumor antigen and a monoclonal anti-idiotype.

We compared the humoral immune responses induced in BALB/c mice by immunization with recombinant SV40 large tumor antigen (T-ag) with those induced by a monoclonal anti-idiotype (anti-Id), designated 58D, that is specific for SV40 T-ag-induced Id network components. We also challenged immunized mice with a lethal dose of SV40-transformed cells to assess in vivo tumor immunity. Two biweekly immunization with either SV40 T-ag or anti-Id 58D induced humoral responses that recognized both SV40 T-ag and anti-Id 58D. Four biweekly immunizations with SV40 T-ag increased the antigen-specific antibody titers and decreased the response to anti-Id 58D, while four biweekly immunizations of anti-Id 58D increased antibody titers to both itself and SV40 T-ag. Comparison of specific T-ag epitope and idiotope specificities indicated that SV40 T-ag and anti-Id 58D immunization generated responses that recognized a similar epitope on SV40 T-ag and expressed a shared idiotope recognized by anti-Id 58D. SV40 T-ag immunized mice challenged with a lethal dose of SV40-transformed cells were completely protected and no tumors were observed. This is despite the fact that little or no SV40 T-ag-specific cytotoxic T-lymphocyte activity was detectable. In contrast, only 3 of 10 mice immunized with anti-Id 58D were protected from a lethal challenge. These results indicate that, although monoclonal anti-Id immunization can induce responses that recognize similar SV40 T-ag epitopes and express shared idiotopes associated with antibodies to SV40 T-ag, the recombinant antigen itself induces superior in vivo tumor immunity.

Animals↗

PubMed1986

Cells involved in the immune response. XXXIII. Antibody-forming cells in the popliteal lymph nodes in the immunized splenectomized rabbit following intravenous immunization and their subsequent dissemination to the thymus.

Rabbits were splenectomized (splx) and immunized intravenously (iv) with sheep erythrocytes (SRBC) 14 days later. At the height of the primary immune response on Day 8 postimmunization, significant numbers of plaque-forming cells (PFC), that is, antibody-forming cells (AFC) synthesizing and secreting antibodies, were detected in the popliteal lymph nodes (PLN) and lesser numbers were detected in the bone marrow and the circulation. No PFC were detected in any of the other lymphoid organs. Rabbits were sacrificed at 1, 2, 6, or 9 months post-primary iv immunization and cell cultures of the lymphoid organs were set up with the antigen, SRBC, to induce secondary immune responses in vitro. Only the PLN cells challenged with SRBC in vitro 1 month post-primary immunization generated PFC and only PLN and thymus cells generated PFC in vitro at the three other challenge periods, thus demonstrating the existence of memory cells in only these two lymphoid organs in the splx rabbits. Following in vivo secondary immunization iv with SRBC 2, 6, or 9 months post-primary iv immunization. PFC were consistently detected only in the PLN and the bone marrow and inconsistently in the circulation. No PFC were detected in the thymus or in any of the other lymphoid organs. Paradoxically, neither the bone marrow nor the circulating mononuclear cells of these rabbits generated PFC during in vitro culture with SRBC, whereas the thymus cells and the PLN cells generated many PFC in culture with SRBC. These results demonstrate that the thymus contains memory cells following primary immunization of the splx rabbit which are not accessible to particulate antigens injected intravenously, possibly due to a blood-thymus barrier to particulate antigen, and therefore cannot be activated in vivo into secondary antibody formation. The results also indicate that the AFC detected in the circulation and in the bone marrow following primary iv immunization, which do not generate PFC in antigen-stimulated cultures in vitro, are degenerating cells whereas the AFC in the PLN and thymus, which generate many PFC in antigen-stimulated cultures in vitro, constitute the noncirculating precursors of the long-lived memory cells in the splx rabbit. This role of the thymus and PLN as reservoirs for memory cells in the immunized splx rabbit is not influenced by nor is it a result of splx since the thymus and PLN have both been shown to be the major sources of memory cells, along with the spleen, in the immunized nonsplx rabbit.

Animals↗

PubMed1974

Immunity to influenza in ferrets. XI. Cross-immunity between A/Hong Kong/68 and A/England/72 viruses: serum antibodies produced by infection or immunization.

The degree of immunity due to cross-reactions between antibody to influenza virus A/Hong Kong/1/68 and A/England/42/72 was studied in ferrets. Ferrets were immunized with the viruses by either live infection or by inoculation with inactivated virus vaccines. The vaccines were given with Freund's incomplete adjuvant or were given to ferrets previously infected with influenza virus A/PR/8/34. As a result of these immunizations the animals all produced similar titres of serum HI antibody to the immunizing virus, although the degree of cross-reaction with the other virus strain was variable. After immunization the animals were challenged by infection with an A/Eng/42/72-like virus and their degree of immunity was measured. It was found that the greatest immunity was in ferrets previously infected with the homologous A/Eng/42/72 virus. Animals previously infected with A/HK/68 virus also showed a measurable degree of immunity to A/Eng/42/72 infection, and this was greater than that found in animals given inactivated virus vaccines. The immunity produced by the vaccines was approximately equal, regardless of which vaccine or method of immunization was used. Thus, live infection produced a more effective, broader immunity than did the use of inactivated virus vaccines.

Animals↗

PubMed1986

Effects of anti-schistosomal chemotherapy on immune responses, protection and immunity. II. Concomitant immunity and immunization with irradiated cercariae.

Resistance of mice to challenge infections of Schistosoma mansoni was evaluated before and after elimination of their primary, established S. mansoni infections with the chemotherapeutic drug praziquantel. Mice treated after either 10 or 20 weeks of primary infection were challenged 6 or 10 weeks after treatment. Mice infected for for 10 weeks prior to treatment expressed progressively less resistance 6 and 10 weeks after treatment. By 10 weeks after treatment significant levels of protection were no longer observed. Resistance waned more slowly if mice were treated 20 weeks after infection, and there was still significant expression of resistance to challenge 10 weeks after treatment. A separate set of experiments evaluated the use of highly irradiated cercariae as a vaccine in mice that had been previously infected with S. mansoni and cured with praziquantel. It was observed that effective immunizations were possible in previously infected mice. These studies demonstrate that established resistance waned after treatment and the rate of loss of protection was dependent upon the duration of infection prior to treatment. Furthermore, the irradiated cercarial vaccine studies indicate that in the murine model induction of immunological resistance was feasible following chemotherapeutic treatment of infected populations.

Animals↗

PubMed1994

Kinetics of the immune response and regression of metastatic lesions following development of humoral anti-high molecular weight-melanoma associated antigen immunity in three patients with advanced malignant melanoma immunized with mouse antiidiotypic monoclonal antibody MK2-23.

Active specific immunotherapy has been implemented in patients with advanced malignant melanoma, utilizing the mouse antiidiotypic (anti-id) monoclonal antibody (mAb) MK2-23 which bears the internal image of high molecular weight-melanoma associated antigen (HMW-MAA). In a previous study, development of anti-HMW-MAA immunity in patients with advanced malignant melanoma immunized with anti-id mAb MK2-23 was found to be associated with a statistically significant survival prolongation. Since no information is available about the relationship between development of immunity and clinical response in patients immunized with anti-id mAb, the present study has characterized the kinetics of the immune response in three patients with advanced malignant melanoma who experienced regression of metastatic lesions following immunization with the anti-id mAb MK2-23. The three patients developed anti-mouse IgG antibodies, anti-anti-id antibodies and anti-HMW-MAA antibodies. The anti-HMW-MAA antibodies are mainly IgG, suggesting that the immune response elicited by anti-id mAb MK2-23 is T-cell dependent. The development of anti-HMW-MAA immunity preceded the reduction in the size of metastatic lesions. This temporal relationship suggests but does not prove that the anti-HMW-MAA immunity elicited by anti-id mAb MK2-23 has a beneficial effect on the clinical course of the disease in patients with malignant melanoma. This finding in conjunction with minor side effects associated with repeated administrations of mouse anti-id mAb MK2-23 suggest that active specific immunotherapy with anti-id mAb which bear the internal image of melanoma-associated antigen represents a viable therapeutic approach to malignant melanoma.

Aged↗

PubMed1984

Generation and decay of the immune response to a progressive fibrosarcoma. II. Failure to demonstrate postexcision immunity after the onset of T cell-mediated suppression of immunity.

This study shows that surgical removal of the meth A fibrosarcoma from its semisyngeneic host fails to result in postexcision immunity to growth of a tumor implant unless the host already has acquired a mechanism of concomitant immunity to growth of an implant. Therefore, tumor excision does not cause immunity to be generated but preserves a mechanism of concomitant immunity that already exists and which otherwise would eventually undergo down-regulation under the influence of suppressor T cells. Removal of the tumor after it has grown large enough to cause the T cell-mediated suppression of concomitant immunity does not result in the reemergence of immunity. Instead, the host remains unable to generate concomitant immunity to a second tumor for a long period of time and retains, for at least 31 d, suppressor T cells able to passively transfer suppression to appropriate recipients. Like the suppressor T cells responsible for active suppression of concomitant immunity, the suppressor T cells responsible for "memory" suppression are of the Ly-1+2- phenotype. The results indicate that progressive tumor growth results in a state of immunological tolerance of tumor-specific, transplantation antigens that can persist in the apparent absence of tumor antigens.

Animals↗

PubMed1977

Immune response to immunization via the anterior chamber of the eye. I. F. lymphocyte-induced immune deviation.

The immunizing abilities of alloantigens placed within the anterior chamber of the eye have been studied in inbred rats. Although intracameral inoculation of F1 hybrid lymphocytes into parental strain recipients elicited both cell- and antibody-mediated immunity, a delimited interval was identified postinoculation during which the systemic cell-mediated immune response was suppressed as indicated by prolonged acceptance of orthotopic skin allografts. The prompt appearance of hemagglutinating antibodies in the serum of immunized rats followed a time course which coincided with the suppression of cell-mediated immunity and suggested that the two events are casually related. Since exposure to allogeneic antigens on lymphoid cells via the anterior chamber elicits a transient suppression in cell-mediated immunity, where humoral immunity is preserved, the phenomenon resembles immune deviation.

Animals↗

PubMed1982

Rubella immunity in older children, teenagers, and young adults: a comparison of immunity in those previously immunized with those unimmunized.

Because rubella continues to be a common illness in adolescents and young adults and because it has been suggested that booster rubella immunizations should be performed, we studied antibody prevalence in 459 predominantly adolescent patients in a pediatric group practice. Rubella antibody (PHA titer greater than or equal to 1:13.5) in previously immunized patients (89.6% of 385) was significantly more common than antibody in unimmunized patients and patients with a questionable history of immunization (70.3% of 74) (P less than 0.005). Twenty-three seronegative patients with a documented history of prior immunization were reimmunized and 22 had an IgG (secondary) antibody response and only one an IgM (primary) antibody response. Since all but one of our patients with previous immunization had a secondary immune response following revaccination, it seems likely that the level of protection in previously vaccinated individuals is considerably greater than 90%. Attention today should be directed at finding and immunizing unvaccinated teenagers and young adults and not in major booster vaccine programs.

Adolescent↗

PubMed1972

Specific immune response genes of the guinea pig. V. Influence of the GA and GT immune response genes on the specificity of cellular and humoral immune responses to a terpolymer of L-glutamic acid, L-alanine, and L-tyrosine.

The ability of guinea pigs to make immune responses to the random linear copolymer of L-glutamic acid and L-alanine, GA, and to L-glutamic acid and L-tyrosine, GT, is each controlled by a different immune response gene. On the other hand, the random linear terpolymer of L-glutamic acid, L-alanine, and L-tyrosine, GAT, which contains both GA and GT antigenic determinants, is immunogenic in all guinea pigs. After GAT immunization, all animals develop delayed hvpersensitivity and serum antibody specific for GAT. However, only those guinea pigs possessing the GA immune response gene demonstrate cross-reactive delayed hypersensitivity when challenged with GA. In addition, the anti-GAT antisera produced by those animals having the GA gene contain cross-reacting anti-GA antibodies. The sera from guinea pigs lacking the GA gene have no anti-GA antibody activity. Thus, we have demonstrated that a specific immune response gene controlling responsiveness to a "simple" antigen can determine the specificity of both cellular and humoral immune responses to a more complex antigen.

Alanine↗

PubMed1993

Immunization status and reasons for immunization delay among children using public health immunization clinics.

OBJECTIVES: To determine whether children attending our local health department clinics were being immunized in a timely manner, and to investigate the reasons for children not being immunized on schedule. DESIGN: Cross-sectional research design. SETTING: Five Salt Lake City/County Health Department immunization clinics in Utah. PARTICIPANTS: All patients presenting to the clinics for immunization from November 1990 to March 1991 when minor illness is prevalent. INTERVENTIONS: Data were gathered through interview and questionnaire. MEASUREMENTS/MAIN RESULTS: Children were mostly white; they came from two-parent households with reasonably high incomes and high parental education level. Only four children were denied vaccination, all for inappropriate timing. None were denied for illness. More than 75% had postponed bringing their children in for immunization. The most common reason given for delay was minor illness in the child. CONCLUSION: Even in this "low-risk" population, parental misperception regarding immunizations is a significant, contributing factor to low immunization rates. Public educational programs directed at increasing parental knowledge must be developed.

Child, Preschool↗

PubMed1985

Prophylactic immunization against experimental leishmaniasis. IV. Subcutaneous immunization prevents the induction of protective immunity against fatal Leishmania major infection.

Durable immunity against fatal L. major infection in genetically susceptible mice can be induced by immunization with 150,000-rad irradiated or heat-killed promastigotes administered i.v. or to a lesser extent i.p. Conversely, subcutaneous (s.c.) and intramuscular (i.m.) injections are not only totally ineffective but generally increase susceptibility to and enhance the progression of the disease, leading to earlier mortality. This detrimental effect is particularly evident with lower infecting challenge doses. Disease exacerbation is apparent in mice given 4 X s.c. injections of as few as 2 X 10(4) irradiated promastigotes, but it appears most potent after doses of 2 X 10(7). When mice given 4 X s.c. injections were subsequently immunized i.v. with 2 X 10(7) irradiated promastigotes, they failed to develop any evidence of protection against infection with 2 X 10(5) promastigotes, whereas mice given i.v. immunization alone were strongly protected. Thus, s.c. injections are capable of blocking the prophylactic effect of i.v. immunization with irradiated parasites. This inhibitory effect can be achieved with a single s.c. injection, although rather less potently than with four, and is even effective against four repeated weekly i.v. immunizations. Once induced, the effect persists undiminished after 100 days. A weaker effect is also inducible by s.c. injection given after i.v. immunization. The blocking effect of s.c. injection is not dependent on continuing viability of the promastigotes, as it can be induced equally readily with heat-killed, formalin-fixed, or sonicated parasites. The phenomenon extends to mouse strains genetically resistant as well as susceptible to L. major infection and, in congenic mice of BALB background, is independent of the major histocompatibility (H-2) gene complex.

Animals↗