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PubMed1997

Immune deviation in relation to ocular immune privilege.

Immune privilege in the eye is a dynamic state in which the immune response to ocular Ags is molded and modified by the eye itself. Immune privilege correlates with systemic alterations in the immune response such that deviant forms of immunity emerge. The eye itself contributes to immune deviation, in part by displaying unique immunoregulatory factors in aqueous humor and expressed on ocular cells. When T cells encounter Ag in the eye, they can become anergic, undergo apoptosis, secrete TGF-beta, and/or release soluble regulatory factors containing the TCR alpha-chain. Ags taken up by indigenous APC escape the eye and reach the spleen where they activate a unique spectrum of Ag-specific T and B cells. The absence of systemic delayed hypersensitivity and complement-fixing Abs in this deviant response probably relates to the fact that inflammation is deleterious to vision and leads to blindness. Immune privilege is the eye's way of protecting its vital function from the ravages of immunopathogenic injury.

Animals↗

PubMed1999

Immunization of melanoma patients with BEC2-keyhole limpet hemocyanin plus BCG intradermally followed by intravenous booster immunizations with BEC2 to induce anti-GD3 ganglioside antibodies.

BEC2 is an anti-idiotypic mouse monoclonal antibody that mimics GD3 ganglioside. Previous clinical trials demonstrated that intradermal immunization using 2.5 mg of BEC2 with BCG or i.v. immunization with 10 mg of BEC2 can induce anti-GD3 antibodies in a subset of patients. We hypothesized that combining these two immunization strategies might be more effective in inducing anti-GD3 antibodies and that conjugation of BEC2 to keyhole limpet hemocyanin (KLH) would further enhance the immunogenicity of BEC2. In this clinical trial, 18 melanoma patients who were free of disease after complete surgical resection within 1-6 months received intradermal immunizations on weeks 0, 2, 4, 6, and 10 with 2.5 mg of BEC2 conjugated to KLH and mixed with BCG (BEC2-KLH/BCG). Booster immunizations of 10 mg of unconjugated BEC2 were administered i.v. on weeks 24, 37, and 50. Four of 18 patients (22%) developed IgM anti-GD3 antibodies. No IgG anti-GD3 antibodies were detected. All four responding patients developed anti-GD3 IgM during immunization with BEC2-KLH/BCG; only one patient demonstrated a reboost of the IgM anti-GD3 titer during the i.v. immunizations. Thirteen of the patients are free of melanoma (3 after undergoing re-resection for local relapse); 14 patients (78%) remain alive with a median follow-up of 28 months. These results confirm our previous trial, showing that BEC2 with BCG can induce anti-GD3 antibodies in patients. The data do not provide evidence that conjugation to KLH increases the immunogenicity of BEC2 when it is administered with BCG.

Adjuvants, Immunologic↗

PubMed1999

Induction of protective host immunity to carcinoembryonic antigen (CEA), a self-antigen in CEA transgenic mice, by immunizing with a recombinant vaccinia-CEA virus.

Human carcinoembryonic antigen (CEA) is a well-characterized oncofetal glycoprotein whose overexpression by human carcinomas has been a target for cancer immunotherapy. Transgenic mice that express CEA as a self-antigen with a tissue distribution similar to that of humans have been developed. This study investigates: (a) the responsiveness of the CEA transgenic (CEA.Tg) mice to endogenous CEA or CEA administered as a whole protein in adjuvant; and (b) whether the presentation of CEA as a recombinant vaccinia virus could generate CEA-specific host immunity. By and large, the CEA.Tg mice were unresponsive to CEA, as shown by the lack of detectable CEA-specific serum antibodies and the inability to prime an in vitro splenic T-cell response to CEA. Furthermore, the administration of whole CEA protein in adjuvant to CEA.Tg mice failed to elicit either anti-CEA IgG titers or CEA-specific T-cell responses. Only weak anti-CEA IgM antibody titers were found in those mice. In contrast, CEA.Tg mice immunized with recombinant vaccinia virus expressing CEA generated relatively strong anti-CEA IgG antibody titers and demonstrated evidence of immunoglobulin class switching. These mice also developed T(H)1-type CEA-specific CD4+ responses and CEA peptide-specific cytotoxicity. The ability to generate CEA-specific host immunity correlated with protection of the CEA.Tg mice against a challenge with CEA-expressing tumor cells. Protection against tumor growth was accomplished with no apparent immune response directed at CEA-positive normal tissue. The results demonstrate the ability to generate an effective antitumor immune response to a tumor self-antigen by immunization with a recombinant vaccinia virus. CEA.Tg mice should be an excellent experimental model to study the effects of more aggressive immunization schemes directed at established tumors with the possible development of accompanying autoimmune responses involving normal tissues.

Animals↗

PubMed1998

Long-lived protective immunity to Listeria is conferred by immunization with particulate or soluble listerial antigen preparations coadministered with IL-12.

The ability of IL-12 to promote the development of Th1-type immune responses, and thus promote cellular immunity, has been well documented. In a previous report, we showed that coadministration of IL-12 with heat-killed Listeria monocytogenes elicited intense antigen-specific T cell responses that conferred protective listerial immunity. Herein, we have extended those studies by demonstrating that multiple injections of heat-killed L. monocytogenes and IL-12 elicit memory responses that confer long-lived (> or = 3 months) protective immunity and that immunity can be transferred adoptively with cells from immunized mice injected into naive mice. These studies have also demonstrated that the powerful adjuvanticity of IL-12 is observed with soluble as well as particulate immunogens and is operative in mouse strains that have different MHC haplotypes. These findings suggest that IL-12 may be a useful adjuvant component of vaccines for a wide variety of pathogens in animal and human systems.

Adjuvants, Immunologic↗

PubMed1996

Cell-mediated immune response of macaques immunized with low doses of simian immunodeficiency virus (SIV).

Many uninfected people at high risk of HIV infection developed an HIV-specific cellular immune response despite their lack of seroconversion. Therefore, they must have been exposed to HIV without subsequent infection. It has been concluded from these data, that cell-mediated immunity (CMI) rather than humoral immunity might confer protection to HIV infection. Therefore, we tried to induce such a strong CMI in macaques by different immunization strategies. Five or seven animals were immunized with high or low doses of a whole SIV split vaccine. The lower dose of the vaccine provoked a stronger T-helper cell (TH) proliferation than the higher dose, which led to a pronounced humoral immune response. To induce a strong CMI without any specific antibody response, five macaques were inoculated with low doses of infectious SIV. None of these animals seroconverted but each animal developed a SIV-specific TH response. Interestingly, we could neither detect an SIV-specific CTL activity in the animals nor did we find typical TH1- or TH2-like cytokine profiles investigating stimulated bulk-cultures from SIV-exposed animals by RT-PCR. 24 weeks after the first low dose SIV exposure the animals were boosted by a second low dose of SIV followed by a subsequent intravenous challenge with a high dose of SIV 12 weeks later. Unexpectedly, none of the animals was found to be protected against infection and the development of AIDS-like symptoms.

Animals↗

PubMed2003

Measles and mumps vaccination as a model to investigate the developing immune system: passive and active immunity during the first year of life.

Evaluations of neutralizing antibody responses in 6-, 9- and 12-month-old infants given measles or mumps vaccine indicated that 6-month-old infants had diminished humoral immune responses associated with passive antibody effects, but also had an intrinsic deficiency in antiviral antibody production, which was independent of passive antibody effects. In contrast, lower neutralizing antibody titers in 9-month-olds were related only to passive antibody effects. Measles and mumps-specific T-cell proliferation and interferon-gamma (IFNgamma) production were induced by vaccination at 6, 9 or 12 months, regardless of passive neutralizing antibodies or age. These observations suggest a need to refine concepts about passive antibody interference and primary vaccine failure, taking into account the sensitization of antiviral T-cells, which occurs in the presence of passive antibodies and is observed in infants who do not develop active humoral immunity. A second dose of measles vaccine given at 12-15 months enhanced antiviral T-cell responses to measles in infants who were vaccinated at 6 or 9 months, and produced higher seroconversion rates. Since T-cell immunity is elicited under the cover of passive antibodies, the youngest infants benefit from the synergistic protection mediated by maternal antibodies and their own capacity to develop sensitized antiviral T-cells, which prime for subsequent exposures to the viral antigens. Conceptually, maternal immunization approaches with vaccines that can be given to women of child-bearing age before pregnancy, or that are safe for administration during pregnancy, should enhance passive antibody protection. Rather than being detrimental to infant adaptive immune responses, maternal vaccination can be coupled effectively with vaccine regimens that elicit priming of antiviral immune responses in infants during the first year of life.

Aging↗

PubMed1996

Stress-induced suppression of the cellular immune reactions: on the neuroendocrine control of the immune system.

Immune competence is considered as a state of equilibrium between humoral and cellular immunity. This notion fits well with the functionally antagonistic cytokine profiles in cell groups of CD4(+)-helper cells as described by Mosmann and Coffman. The Th-1 cells release mainly IL-2, IL-12 and IFN gamma and thereby stimulate the cellular immune reactions. Conversely, the Th-2 cells produce predominantly IL-4, IL-6 and IL-10, thus enhancing humoral immune reactions. Recently, it has been shown that the lymphokine profiles in Th-2 are linked to changes of the humoral balance between cortisol and dehydroepiandrosterone. These studies show that there exist states of equilibrium between T- and B-cell-mediated immune reactions, which may selectively be altered to the disadvantage of the T-cellular immunity by a stress-induced enhancement of cortisol release. In an attempt to restitute stress-induced immunosuppression, a dampening of the cortisol release hormone in the hypothalamus should, therefore, be of primary importance.

Animals↗

PubMed2002

Polyspecific malaria antibodies present at the time of infection inhibit the development of immunity to malaria but antibodies specific for the malaria merozoite surface protein, MSP1, facilitate immunity.

Serum taken from mice immune to malaria as a result of infection and drug cure, or from mice immunized with a recombinant form of the merozoite surface protein, MSP1, can provide passive protection of recipient mice against the lethal parasite, Plasmodium yoelii YM. However, recipients of MSP1-immune serum go on to develop long-term immunity, whereas recipients of serum from mice naturally immune to malaria rapidly lose their resistance to infection. We demonstrate that 'infection/cure' serum suppresses the development of both antibody and cell-mediated parasite-specific responses in recipients, whereas these develop in recipients of MSP1-specific antibodies. These data have profound implications for our understanding of the development of malaria immunity in babies who passively acquire antibodies from their mothers.

Animals↗

PubMed2003

Successful induction of CD8 T cell-dependent protection against malaria by sequential immunization with DNA and recombinant poxvirus of neonatal mice born to immune mothers.

In some parts of Africa, 50% of deaths attributed to malaria occur in infants less than 8 mo. Thus, immunization against malaria may have to begin in the neonatal period, when neonates have maternally acquired Abs against malaria parasite proteins. Many malaria vaccines in development rely upon CD8 cells as immune effectors. Some studies indicate that neonates do not mount optimal CD8 cell responses. We report that BALB/c mice first immunized as neonates (7 days) with a Plasmodium yoelii circumsporozoite protein (PyCSP) DNA vaccine mixed with a plasmid expressing murine GM-CSF (DG) and boosted at 28 days with poxvirus expressing PyCSP were protected (93%) as well as mice immunized entirely as adults (70%). Protection was dependent on CD8 cells, and mice had excellent anti-PyCSP IFN-gamma and cytotoxic T lymphocyte responses. Mice born of mothers previously exposed to P. yoelii parasites or immunized with the vaccine were protected and had excellent T cell responses. These data support assessment of this immunization strategy in neonates/young infants in areas in which malaria exacts its greatest toll.

Animals↗

PubMed1975

[Effect of immunosuppressive and cytostatic factors on the immune responses of the body. Communication II. Effect of hydrocortisone on immunologically competent cells (RFC cells and lymphocytes B) in immunized animals (author's transl)].

The effect of hydrocortisone on immunologically competent cells in peripheral blood (lymphocytes B and RFC cells) and on the level of humoral antibodies has been studied in rabbits immunized twice with 10per cent sheep erythrocytes. The animals were divided into two groups. The experimental group, numbering 14 rabbits, was administered 30 mg/kg body weight of hydrocortisone intramuscularly for three consecutive days before the first and second dose of antigen; the 10 rabbits of the control group were administered only the antigen. The results obtained showed that, after immunization and in the course of the normal immune response of the body, the numbers of RFC cells and of lymphocytes B increased in peripheral blood before the level of antibodies rose (Fig. 1, 3 and 4). The results in the group of experimental rabbits showed that hydrocortisone markedly suppressed the normal immune response of the body to the antigen administered. When the data obtained in both groups studied were compared, it was found that the amount of RFC cells and of lymphocytes B in peripheral blood was manifestly smaller in the group of experimental animals treated with hydrocortisone, than in the group of control animals, both after the first and the second dose of antigen (Fig. 1, 2 and 3). The difference concerning the humoral antibodies level between the two groups, however, appeared only after the second dose of the antigen (Fig. 4, Table I). That means that the investigation of immunologically competent cells in peripheral blood, such as lymphocytes B and RFC cells, enables to detect disturbances in the immune response of the body earlier than the investigation of humoral antibodies and supplies a more complete image of the changes occurring in the body during immunization.

Agglutinins↗

PubMed2000

Tolerance and immunity in the intestinal immune system.

The intestinal immune system must guard the body against invasion by pathogens while avoiding a response to the many potential antigens present in food. In the absence of the inflammatory stimuli necessary to elicit an immune response, oral administration of soluble protein antigens induces antigen-specific systemic nonresponsiveness. Recent studies have shown that peripheral nonresponsiveness to orally administered antigen is preceded by transient T-cell activation and is due primarily to the induction of functional T-cell anergy. The microenvironment of the gut-associated lymphoid tissue plays a central role in orally induced nonresponsiveness by supporting the growth of regulatory T cells that maintain intestinal homeostasis in the face of constant antigenic challenge. The transfer of nonresponsiveness by peripheral T cells from antigen-fed mice suggests that these-gut-derived regulatory cells also function in peripheral sites. When oral antigens are presented with adjuvants (microbial products that activate the innate immune system) an adaptive immune response is induced to this normally tolerogenic form of antigen. This review examines recent work that has provided new insight into the regulation of tolerance and immunity in the intestinal immune system.

Animals↗

PubMed1979

Influence of different routes of anti-tumor immunization: alternative induction of tumor immunity and tumor enhancement.

Chickens and quails were immunized in parallel either i.v. or intramuscularly (i.m.) with lectin column-purified antigens from chick embryo cells that were transformed in vitro by avain sarcoma virus (ASV). After five to six injections, immunity of the animals was tested by challenge with ASV into the wing webs. Whereas tumor growth was inhibited after i.v. immunization with respect to incidence rate and time of tumor appearance, tumor growth was enhanced after i.m. injection. Animals that were injected with normal cell antigens served as controls. Spleen cells from only those animals that were immunized i.v. exerted a cytotoxic effect in vitro against ASV-transformed cells, whereas spleen cells from i.m. injected animals, in contrast, suppressed such cytotoxicity. The search for serum blocking or arming factors suggested that sera from i.m. injected animals block cellular cytotoxicity whereas sera from i.v. immunized animals render normal spleen cells cytotoxic (arming effect). The use of viruses from different subgroups and of antigens from gp85-lacking ASV-transformed cells indicates that immune effects were obtained against tumor cell surface antigens that differ from the antigen that is involved in virus neutralization (s-gp85).

Alpharetrovirus↗

PubMed1989

General recommendations on immunization. Guidelines from the Immunization Practices Advisory Committee. Centers for Disease Control.

This revision of the "General Recommendations on Immunization" updates the 1983 statement. Changes or new sections include 1) listing of vaccines available in the United States by type and recommended routes, 2) updated schedules for immunizing infants and children, 3) clarification of the guidelines for spacing administration of immune globulin preparations and different vaccines, 4) an updated table of recommendations for routine immunization of children infected with human immunodeficiency virus, 5) listing of conditions that are often inappropriately considered contraindications to immunizations, and 6) addition of information on the National Childhood Vaccine Injury Act of 1986 and the National Vaccine Injury Compensation Program. These recommendations are not comprehensive for each vaccine: Immunization Practices Advisory Committee (ACIP) recommendations on each vaccine should be consulted for more details.

Adolescent↗

PubMed1984

Cell-mediated immunity in experimental murine dermatophytosis. II. Adoptive transfer of immunity to dermatophyte infection by lymphoid cells from donors with acute or chronic infections.

An in vivo adoptive cell transfer system was used to investigate protective immunity during experimental murine dermatophytosis due to Trichophyton quinckeanum. Using sublethally (550R) irradiated BALB/c mice which are particularly susceptible to infection, it was found that regional lymph node cells from syngeneic acutely-infected donors conferred protection to irradiated recipients. By contrast, serum from the same donors did not prevent infection of normal BALB/c mice. The capacity of lymphoid cells to transfer adoptive immunity was lost after treatment with monoclonal anti-Thy-1.2 antibody and complement, but not after treatment with monoclonal anti-Ly 2.2 antibody and complement, indicating that cellular immunity is mediated by Ly 2-T cells. The cellular activity of chronically infected mice was also studied. Paradoxically, lymphoid cells from these animals which appeared to be immunologically compromised did, however, confer immunity. Adoptive immunity was abrogated by serum from chronically infected donors or by specific dermatophyte antigen, but not by homologous or heterologous anti-dermatophyte antiserum. These findings indicate that competition between cell-mediated immunity and humoral factors may be the causative mechanism for persistence of dermatophyte infection in this system.

Acute Disease↗

PubMed1982

Cutaneous basophil-associated resistance to ectoparasites (ticks). I. Transfer with immune serum or immune cells.

Immune resistance experiments were carried out in guinea-pigs employing two tick species that as adults are ectoparasites of cattle (Ixodes holocyclus and Rhipicephalus appendiculatus). These studies showed that susceptibility of non-immune guinea-pigs to infestation with tick larvae varies according to the species of tick and the strain of guinea-pig. With both tick species, greater than 90% acquired resistance was achieved in several guinea-pig strains. Immune resistance was evident within a week following primary infestation and lasted up to 9 months following a single sensitizing exposure to tick feeding. The strength and duration of resistance was influenced strongly by the size of the initial sensitizing dose. Immune resistance was readily transferred to naive recipients by intravenous administration of either peritoneal exudate cells or immune serum from donors sensitized by a single prior infestation with ticks. Doses of serum as small as 0.5 ml transferred resistance. These studies demonstrate that both sensitized cells and immune serum factors contribute significantly to acquired host resistance to ticks that as adults are ectoparasites of cattle.

Animals↗

PubMed1976

Humoral immunity in experimental syphilis. I. The demonstration of resistance conferred by passive immunization.

Evidence of a role for human factor(s) in immunity to experimental syphilis has been provided by the demonstration that passive immunization of rabbits by daily i.v. injections of immune serum significantly delays the appearance and markedly diminishes the severity and duration of lesions which develop after challenge with Treponema pallidum. Five rabbits were injected daily over 37 days with 3 ml/kg body weight of pooled immune rabbit serum injection with 1.1 X 10(3) T. pallidum, Nichols strain, at each of four sites. The animals developed atypical lesions of short duration after an average delay in onset of 28 days short duration after an average delay in onset of 28 days beyond the development of typical lesions in control animals similarly injected with nonimmune serum or saline. The failure of passive immunization to provide complete protection was evident not only in the development of the atypical lesions, but also in the demonstration of disseminated infection in the tissues of three of the four surviving animals 7 months after challenge. The possibility that incomplete protection may have been due to 1) insufficient immune serum levels, 2) intracellular location of T. pallidum, and/or 3) cell-mediated mechanisms is discussed.

Animals↗

PubMedDate not supplied

[The immunity indices of animals immunized with the inactivated Marburg virus after infection with homologous virus].

The data on changes in the parameters of specific and nonspecific immunity after challenge of the immunized animals with Marburg virus are presented. Mediators of the immune response: tumor necrosis factor, interferon, were shown to play different roles in the development of the disease and "protection" of animals. The survival rate of the immunized animals after the challenge with Marburg virus was determined by the intensity and level of the immune response after challenge rather than by the levels of postvaccination immunity at the time of the challenge.

Animals↗

PubMed1977

Immune responses to influenza virus in rabbits after local immunization. II. Local and systemic cell mediated response.

The development of local and systemic cell mediated immunity (CMI) was investigated in rabbits after intratracheal immunization with live or inactivated influenza A virus. Lymphocytes from bronchoalveolar washings and draining lymph nodes were used for the assay of local CMI response. Spleen cells were employed for determination of systemic responses. Since alveolar macrophages were found to be susceptible to the action of migration inhibiting factor, the development of CMI in lungs was assayed by macrophage migration inhibition test using bronchoalveolar was cells. Immunization with live virus induces beter local CMI response than inactivated virus. After primary immunization the peak responses were found between second and third week. The secondary response was detectable much earlier and peaked at one week after booster. Small amounts of inactivates virus, which was unsufficient to evoke a primary response, could elicit a strong secondary response. The development of rapid and accentuated secondary response in the local lymphoid tissues suggests the presence of memory in the local CMI response. The results also show a good correlation to exist between primary local CMI response and the skin reactivity to the immunizing antigen. However, lack of such correlation during the secondary response leaves the skin tests less reliable in the evaluation of CMI in viral infections. Some of the functions of alveolar macrophages in the local immune reponses are also discussed.

Animals↗