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At least 721 records · Page 40Linked to original sources
PubMed2006

Immune cell migration as a means to control immune privilege: lessons from the CNS and tumors.

Certain organs, such as the brain, eye, and gonads, are particularly sensitive to damage by inflammation. Therefore, these tissues have developed unique immunological properties that curtail inflammatory responses, a phenomenon termed immune privilege. In addition, by co-opting some of the regulatory cues operant in immune privilege in normal organs, tumors can evade immunosurveillance. While many different mechanisms contribute to immune privilege, there is evidence that leukocyte migration is an important checkpoint in its control. This hypothesis is based on the fact that leukocyte entry into these organs is restricted by physical barriers and that the collapse of these obstacles marks a critical step in the development of inflammatory/autoimmune disease at these sites. Numerous studies in a variety of experimental systems have characterized the molecular and cellular mechanisms involved in leukocyte homing to immune-privileged organs. Recently, two-photon microscopy has revealed critical insights into the events occurring in the extravascular space of immune-privileged organs, including locomotion patterns and interactive behavior of leukocytes in the interstitial space. Here, we review our current understanding of immune cell migration to and within immune-privileged organs and highlight how this knowledge may be exploited for immunotherapeutic purposes.

Animals↗
PubMed1986

Cross-reactive lymphocyte responses and protective immunity against other spotted fever group rickettsiae in mice immunized with Rickettsia conorii.

Lymphocyte proliferation in response to antigens on spotted fever group rickettsiae was used as a method to investigate the group-specific protective immunity to rechallenge characteristic of this group of rickettsiae at the T-cell receptor level. Spleen cells from Rickettsia conorii-immune C3H/HeJ mice proliferated in response to R. rickettsii Sheila Smith, R. sibirica 246, R. australis, and all tested strains of R. conorii (Casablanca, Moroccan, and Malish). Spleen cells from these mice, however, responded poorly or not at all to antigens prepared from the Kaplan or Hartford strain of R. akari. Proliferation of immune T cells maintained as in vitro cell lines showed a similar pattern of reactivity to these antigens; however, response to R. akari was consistently demonstrable. Spleen cells from C3H/HeJ mice immunized with R. akari responded to R. akari and R. conorii antigens as well as antigens from the other spotted fever group rickettsiae. Lymphocytes obtained from lymph nodes draining foot pads infected with R. conorii or R. akari demonstrated cross-reactivity similar to that found with immune spleen cells. If immunization was accomplished with R. conorii antigen emulsified in Freund complete adjuvant, the resulting lymph node cells were able to respond to R. akari antigens. These data suggest that infection with R. conorii induces a population of T lymphocytes that recognize an antigen(s) that also is found on other spotted fever rickettsiae and that may be responsible for cross-protective immunity. This antigen probably is not a major antigen on R. akari.

Animals↗
PubMed1999

Protective immunity against Streptococcus mutans infection in mice after intranasal immunization with the glucan-binding region of S. mutans glucosyltransferase.

Here we present the construction and characterization of a chimeric vaccine protein combining the glucan-binding domain (GLU) of the gtfB-encoded water-insoluble glucan-synthesizing glucosyltransferase enzyme (GTF-I) from Streptococcus mutans and thioredoxin from Escherichia coli, which increases the solubility of coexpressed recombinant proteins and stimulates proliferation of murine T cells. The protective potential of intranasal (i.n.) immunization with this chimeric immunogen was compared to that of the GLU polypeptide alone in a mouse infection model. Both immunogens were able to induce statistically significant mucosal (salivary and vaginal) and serum responses (P < 0.01) which were sustained to the end of the study (experimental day 100). Following infection with S. mutans, sham-immunized mice maintained high levels of this cariogenic organism ( approximately 60% of the total oral streptococci) for at least 5 weeks. In contrast, animals immunized with the thioredoxin-GLU chimeric protein (Thio-GLU) showed significant reduction (>85%) in S. mutans colonization after 3 weeks (P < 0.05). The animals immunized with GLU alone required 5 weeks to demonstrate significant reduction (>50%) of S. mutans infection (P < 0.05). Evaluation of dental caries activity at the end of the study showed that mice immunized with either Thio-GLU or GLU had significantly fewer carious lesions in the buccal enamel or dentinal surfaces than the sham-immunized animals (P < 0.01). The protective effects against S. mutans colonization and caries activity following i.n. immunization with GLU or Thio-GLU are attributed to the induced salivary immunoglobulin A (IgA) anti-GLU responses. Although in general Thio-GLU was not significantly better than GLU alone in stimulating salivary IgA responses and in protection against dental caries, the finding that the GLU polypeptide alone, in the absence of any immunoenhancing agents, is protective against disease offers a promising and safe strategy for the development of a vaccine against caries.

Administration, Intranasal↗
PubMed1998

Effect of passive immunization or maternally transferred immunity on the antibody response to a genetic vaccine to rabies virus.

A plasmid vector, termed pSG5rab.gp, expressing the glycoprotein of rabies virus was tested in young adult or neonatal mice in the presence of maternally transferred immunity or passively administered antibodies to rabies virus for induction of an antibody response. Mice born to rabies virus-immune dams developed an impaired antibody response to genetic immunization at 6 weeks of age, as had been previously observed upon vaccination with an inactivated viral vaccine. Similarly, mice passively immunized with hyperimmune serum showed an inhibited B-cell response upon vaccination with the pSG5rab.gp vector, resulting in both cases in vaccine failures upon challenge with a virulent strain of rabies virus. In contrast, the immune responses of mice vaccinated as neonates in the presence of maternal immunity or upon passive immunization to rabies virus with the pSG5rab.gp construct were only marginally affected.

Animals↗
PubMed2004

Intranasal immunization with inactivated influenza virus enhances immune responses to coadministered simian-human immunodeficiency virus-like particle antigens.

Intranasal immunization with inactivated influenza virus vaccine can provide protective immunity, whereas many other antigens are less effective when used for mucosal immunization. To determine whether influenza virus could enhance immune responses to an antigen coadministered to a mucosal surface, we studied the intranasal immunization of mice with a mixture of simian-human immunodeficiency virus (SHIV) virus-like particles (VLPs) and inactivated influenza virus. Compared to mice immunized with SHIV VLPs alone, mice coimmunized with SHIV VLPs and inactivated influenza virus showed significant increases in serum immunoglobulin G (IgG) and mucosal IgA antibodies specific to the human immunodeficiency virus envelope protein, neutralizing activities, numbers of gamma interferon- and interleukin 4-secreting lymphocytes, and cytotoxic-T-lymphocyte activities. The levels of enhancement of immune response by coimmunization with inactivated influenza virus were equivalent to those induced by inclusion of immunostimulatory CpG oligodeoxynucleotides (CpG DNA). We also observed that SHIV VLPs bind to influenza virus virions, forming mixed aggregates. These results indicate that inactivated influenza virus can play a role as a mucosal adjuvant to coadministered antigens.

AIDS Vaccines↗
PubMed1980

Cellular immunity induced by lung immunization of Fischer 344 rats.

This study describes immunologic response in lung-associated lymph nodes, spleen, cervical lymph nodes and lung lavage cells of rats immunized by intratracheal instillation of BCG-sheep red blood cell (SRBC) suspensions. At 4 through 17 days after immunization, the number of anti-SRBC IfM and IgG antibody-forming cells was significantly increased only in the lung-associated lymph nodes, indicating that these tissues retain the particulate antigen that was deposited in the lung. In contrast, cellular immunity was found initially in the spleen, with significant responses in the lungs and in the lung-associated lymph nodes on 13--19 days after immunization. Our data indicated that the lung-associated lymph nodes are probably the initial site for the production of antigen-sensitive lymphocytes for both antibody and cellular immunity after lung immunization. Cells responsible for cellular immunity appear to migrate to the spleen, where further cell division take place.

Animals↗
PubMed1976

Cellular and humoral bronchopulmonary immune response of rabbits immunized with thermophilic actinomyces antigen.

The immunologic events involved in the pathogenesis of human hypersensitivity pneumonitis are poorly understood. To delineate better the cellular and humoral bronchopulmonary response to host challenge with an important agent for hypersensitivity pneumonitis, an animal model was developed. Rabbits intratracheally inoculated with Micropolyspora faeni antigen developed histologic lesions resembling hypersensitivity pneumonitis in man, characterized by a mononuclear cell interstitial reaction and a marked increase in the number of intra-alveolar cells. This reaction was intense 8 days after immunization and progressively decreased in intensity, with complete resolution occurring, in some instances, by 3 weeks. The increased intra-alveolar cells were predominantly macrophages, but soon after immunization, greater numbers of lymphocytes and granulocytes were present. Associated with the intra-alveolar macrophage response was the appearance of "activated" macrophages, based on increased glucose oxidation and ultrastructural appearance. The immunized rabbits demonstrated Arthus-type skin reactions, as well as delayed hypersensitivity skin reactions after intradermal injection of M. faeni antigen. Alveolar macrophage migration was significantly inhibited in immunized rabbits in the presence of M. faeni antigen, suggesting that specifically sensitized lymphocytes were present in the free bronchoalveolar cell population. Intratracheal inoculation with M. faeni resulted in the production of anti-M. faeni-precipitating antibodies in the sera of all animals and in bronchoalveolar secretions in 15 of 16 inoculated rabbits. The concentrations of IgG and IgA in lung-wash fluid were significantly greater in immunized animals. In the immunized rabbits, the mononuclear cell response, positive M. faeni-induced direct migration inhibition factor assays, and delayed skin reactivity strongly suggested the presence of a delayed hypersensitivity component in disease pathogenesis. The presence of precipitating antibody and the increased concentrations of immunoglobulins were consistent with stimulation of the humoral immune system; however, the role of humoral mechanisms in the pathogenesis of the pulmonary lesions is less certain than that of delayed hypersensitivity.

Animals↗
PubMed1980

Immune stimulation of lung bactericidal activity: evidence for both cellular and humoral participation after immunization with Serratia marcescens.

Mice were immunized by aerosol or by a parenteral route with Serratia marcescens, and subsequently challenged by aerosol with both Staphylococcus aureus and S. marcescens. After a single aerosol immunization, intrapulmonary bactericidal activity was initially enhanced against both organisms. Repetitive aerosol immunization caused the same initial response; however, after antistaphylococcal activity returned to normal, enhanced antiserratia activity was still demonstrable. Parenteral immunization was associated with increased in situ bactericidal activity against both organisms with more pronounced antiserratia activity. Intracellular bactericidal activity against S. aureus of lung phagocytes harvested from mice after aerosol immunization with serratia paralleled the above findings. Aerosol immunization also resulted in recruitment of polymorphonuclear leukocytes. These data suggested that macrophage activation, leukocyte recruitment, and local antibody are important contributing factors to heightened lung antibacterial activity after aerosol immunization with S. marcescens.

Animals↗
PubMed2006

Roles of glycans and glycopeptides in immune system and immune-related diseases.

Almost all of the key molecules in organisms involved in the innate and adaptive immune response (including immunoglobulins, cytokines and cytokine receptors, complements, CD molecules, adhesions, T-cell receptors and major histocompatibility complex molecules) are glycoproteins. Besides, foreign antigens, such as many viral envelope proteins, are glycoproteins too. Carbohydrates attached to proteins or peptides are classified by the nature of their linkages to the protein, mostly as either N-linked (N-acetylglucosamine to asparagines) or O-linked (N-acetylgalactosamine to serine or threonine) oligosaccharides. The glycans have three major roles: firstly, the sugars confer stability on the proteins to which they are attached, protecting them from proteases and non-specific protein-protein interactions. Secondly, glycans play key roles in signal transduction, control of cell development and differentiation. Thirdly, specific regions of the oligosaccharide chains provide recognition epitopes, which influence innate and adaptive immune responses. Glycopeptides not only provide specific oligosaccharides, but also have specific information of amino acids sequences. The glycans and glycopeptides not only influence the structure and functions of immune molecules, but also influence the immune response. In addition, changes in glycans or glycopeptides may have a significant role in a variety of human immune-related diseases, such as rheumatoid, autoimmune disease, Wiskott-Aldrich syndrome, infection disease, cancer, etc. In this article, the roles of N-, O-glycans and glycopeptides in immune system and immune-related diseases are discussed. The potential therapeutic significance of the information is also mentioned.

Animals↗
PubMed2026

Cyclin-dependent kinase 4 and 6 inhibitors and the breast cancer immune ecosystem: immune remodeling, resistance, and therapeutic reprogramming.

Cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6 inhibitors) combined with endocrine therapy have become a therapeutic backbone for hormone receptor-positive, human epidermal growth factor receptor 2-negative breast cancer, yet durable disease control is frequently limited by intrinsic and acquired resistance. Canonical tumor-cell mechanisms, including retinoblastoma-pathway escape, cyclin E-cyclin-dependent kinase 2 (CDK2) activation, endocrine adaptation, and phosphoinositide 3-kinase (PI3K)-AKT-mechanistic target of rapamycin (mTOR) signaling, explain only part of this failure because they do not fully capture dynamic immune and stromal remodeling. Preclinical and translational studies indicate that early CDK4/6 inhibition can enhance antigen presentation, activate interferon-related programs, restrain regulatory T cells, and promote a T-cell-inflamed state. These effects are conditional and may not persist during prolonged treatment. Sustained therapy can instead drive heterogeneous resistant niches characterized by stromal remodeling, myeloid recruitment, checkpoint adaptation, and T-cell dysfunction. This immune-state dependence provides a rationale for immune checkpoint blockade, although clinical combinations have shown mixed efficacy and clinically relevant hepatic, pulmonary, and hematologic toxicities. Sequential or lead-in strategies therefore warrant prospective evaluation. Oxidative phosphorylation (OXPHOS) and redox adaptation may sustain selected resistant states and expose context-dependent ferroptotic vulnerabilities. Ferroptosis may connect tumor-cell killing with immune regulation, whereas nanomedicine may improve tumor-selective delivery. Both strategies remain largely preclinical and require further evaluation of pharmacokinetics, biodistribution, toxicity, manufacturability, and immune-cell safety. This Review distinguishes intrinsic from acquired resistance across interpatient, intratumoral, spatial, and temporal dimensions. It integrates tumor-cell escape with cytokine, immune, stromal, vascular, and metabolic remodeling and summarizes emerging therapeutic strategies. We further propose a candidate biomarker-informed framework that integrates genomic profiling, spatial immune architecture, circulating biomarkers, T-cell receptor (TCR) dynamics, transcriptomic and single-cell analyses, artificial intelligence (AI)-assisted multimodal integration, and longitudinal sampling. This framework is intended to support biomarker development and prospective trial design rather than current clinical decision-making, providing a translational basis for testing state-informed and sequence-aware therapeutic strategies.

Humans↗
PubMed1993

Humoral immune responses in volunteers immunized with irradiated Plasmodium falciparum sporozoites.

Volunteers immunized with gamma-irradiated Plasmodium falciparum sporozoites serve as the gold standard for protective immunity against mosquito-borne malaria transmission and provide a relevant model for studying protective immune effector mechanisms. During a 7-12 month period, we immunized four volunteers via the bites of irradiated, infected mosquitoes. Following these exposures to attenuated sporozoites, all four volunteers developed antibodies to sporozoites as measured by an immunofluorescence assay and by an enzyme-linked immunosorbent assay using the circumsporozoite (CS) protein repeat-based molecule R32LR as capture antigen. Three volunteers also developed antibodies against the nonrepeating (flanking) regions of the CS protein; the level of these antibodies paralleled the serum activity to inhibit sporozoite invasion of hepatoma cells in vitro. These three volunteers were protected against malaria transmitted by the bites of five infected mosquitoes. Two of these protected volunteers received additional immunizing doses of irradiated sporozoites and were subsequently protected against challenge with a heterologous P. falciparum clone. No detectable fluctuations were observed in circulating levels of tumor necrosis factor, interferon-gamma, or interleukin-6 during the course of this study. Analysis of the humoral and cellular immune responses of these protected volunteers is expected to yield important clues to additional targets of immunity against the pre-erythrocytic stages of malaria parasites.

Adult↗
PubMed2002

General recommendations on immunization. Recommendations of the Advisory Committee on Immunization Practices (ACIP) and the American Academy of Family Physicians (AAFP).

This report is a revision of General Recommendations on Immunization and updates the 1994 statement by the Advisory Committee on Immunization Practices (ACIP) (CDC. General recommendations on immunization: recommendations of the Advisory Committee on Immunization Practices [ACIP]. MMWR 1994;43[No. RR-1]:1-38). The principal changes include expansion of the discussion of vaccination spacing and timing, recommendations for vaccinations administered by an incorrect route, information regarding needle-free injection technology, vaccination of children adopted from countries outside the United States, timing of live-virus vaccination and tuberculosis screening, expansion of the discussion and tables of contraindications and precautions regarding vaccinations, and addition of a directory of immunization resources. These recommendations are not comprehensive for each vaccine. The most recent ACIP recommendations for each specific vaccine should be consulted for additional details. This report, ACIP recommendations for each vaccine, and other information regarding immunization can be accessed at CDCs National Immunization Program website at http.//www.cdc.gov/nip (accessed October 11, 2001).

Adolescent↗
PubMed2006

Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP).

Routine vaccination of children is an effective way to reduce hepatitis A incidence in the United States. Since licensure of hepatitis A vaccine during 1995-1996, the hepatitis A childhood immunization strategy has been implemented incrementally, starting with the recommendation of the Advisory Committee on Immunization Practices (ACIP) in 1996 to vaccinate children living in communities with the highest disease rates and continuing in 1999 with ACIP's recommendations for vaccination of children living in states, counties, and communities with consistently elevated hepatitis A rates. These updated recommendations represent the final step in the childhood hepatitis A immunization strategy, routine hepatitis A vaccination of children nationwide. Implementation of these recommendations will reinforce existing vaccination programs, extend the benefits associated with hepatitis A vaccination to the rest of the country, and create the foundation for eventual consideration of elimination of indigenous hepatitis A virus transmission. This report updates ACIP's 1999 recommendations concerning the prevention of hepatitis A through immunization (CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices [ACIP]. MMWR 1999:48[No. RR-12]:1-37) and includes 1) new data on the epidemiology of hepatitis A in the era of hepatitis A vaccination of children in selected U.S. areas, 2) results of analyses of the economics of nationwide routine vaccination of children, and 3) recommendations for the routine vaccination of children in the United States. Previous recommendations for vaccination of persons in groups at increased risk for hepatitis A or its adverse consequences and recommendations regarding the use of immune globulin for protection against hepatitis A are unchanged from the 1999 recommendations.

Adult↗
PubMed1991

Immune regulation of mouse 5T2 multiple myeloma. I. Immune response to 5T2 MM idiotype.

The transplantable murine multiple myelomas (MM) of the 5T series originated spontaneously in the aging C57BL/KaLwRij mice. These murine malignancies offer an excellent model for experimental studies on different aspects of the human disease. With the aim to look for new treatment modalities, the influence of idiotype-specific immune response on the 'take' and the development of the 5T2 MM was studied. In the first experiment, long-lasting subcutaneous immunizations of syngeneic mice with the 5T2 MM immunoglobulin (Ig) showed a dose dependent anti 5T2 MM Ig idiotype-specific response. The majority of the optimally immunized mice showed no 'take' or they had a prolonged survival after intravenous inoculation with the 5T2 MM cells. All control mice, nonimmunized or immunized with an irrelevant 5T14 MM Ig, developed 5T2 MM with a typical lethal course. In the second experiment, delayed type hypersensitivity (DTH) reaction to the 5T2 MM idiotype was studied. Subcutaneous immunizations of syngeneic mice with 5T2 MM Ig or with 5T2 MM bone marrow cells resulted in a specific DTH reaction 48 hours after challenge with 5T2 MM bone marrow cells. No DTH reaction was obtained when intravenous immunization was used. These results indicate that 5T2 MM is sensitive to idiotype-specific immune regulation; they constitute a basis for further studies on treatment of already established MM in vivo.

Animals↗
PubMed1990

Immune responses in BALB/c mice following immunization with aromatic compound or purine-dependent Salmonella typhimurium strains.

Two near isogenic strains of Salmonella typhimurium HWSH, stably mutated in either the aroA gene affecting the biosynthesis of aromatic compounds, or the purA gene affecting the biosynthesis of purines, were administered intravenously as live attenuated vaccines to BALB/c mice. HWSH aroA-immunized mice were well protected against intravenous (i.v.) challenge with wild-type virulent HWSH for at least 10 weeks, whereas HWSH purA-immunized mice were unprotected. Furthermore, HWSH aroA-immunized mice could also control a heterologous challenge with virulent Listeria monocytogenes at 7 and 14 days post-immunization, whereas mice receiving a similar dose of HWSH purA could not. Increasing the i.v. dose of HWSH purA compared to HWSH aroA induced some resistance to L. monocytogenes. Induction of early anti-S. typhimurium resistance by HWSH aroA immunization appeared slightly later than the anti-L. monocytogenes resistance. Mice immunized with either vaccine were able to mount S. typhimurium-specific T-cell proliferative responses and produced anti-S. typhimurium humoral antibodies in their serum. The antibody titre was greater in those mice immunized with the aroA mutant.

Animals↗
PubMed1977

Immunity to sporozoite-induced malaria infeciton in mice. I. The effect of immunization of T and B cell-deficient mice.

The cellular basis of immunity to sporozoites was investigated by examing the effect of immunization of T and B cell-deficient C57BL/6N X BALB/c AnN F1 (BLCF1) mice compared to immunocompetent controls. Immunization of T cell-deficient (ATX-BM-ATS) BLCF1 mice with x-irradiated sporozoites did not result in the generation of protective immunity. The same immunization protocols protected all immunocompetent controls. In contrast, B cell-deficient (micron-suppressed) BLCF1 mice were protected by immunization in the majority of cases. The absence of detectable serum circumsporozoite precipitins or sporozoite neutralizing activity in the micron-suppressed mice that resisted a sporozoite challenge suggests a minor role for these humoral factors in protection. These data demonstrate a preeminent role for T cells in the induction of protective immunity in BLCF 1 mice against a P. berghei sporozoite infection.

Animals↗
PubMed1986

[Immune complex binding by erythrocytes and its significance in the destruction of these cells during immunization].

Immunization of BALB/c mice by sheep red blood cells and Salmonella typhi vaccine has been shown to augment the immune complexes in plasma and erythrocytes in blood fixing the immune complexes on their surface. The inactivation of immune complexes in immunized mice by intravenous injection of the antiserum against aggregated immunoglobulins decreases the hemoglobin in blood serum. The data obtained show that the fixation of immune complexes on erythrocytes is one of the reasons of erythrocytes destruction activation in immunization.

Animals↗
PubMed1977

Immune mechanisms to Ascaris suum in inbred guinea-pigs. I. Passive transfer of immunity by cells or serum.

Syngeneic Strain 2 guinea-pigs which received seven s.c. injections of infective eggs of Ascaris suum were shown to harbour less larvae in their lungs than control animals after mesenteric vein challenge with 10,000 infective larvae of A. suum. Serum and cell preparations harvested from these animals were able to transfer protective immunity to normal recipients to varying degrees. Significant protection with serum preparations was obtained with immune IgG2, IgE + IgG1 and whole immune serum. Best protection with cell preparations was obtained with a pool of cells from the mesenteric, hepatic (retropancreatic), and mediastinal nodes of immune animals. Cells from the hepatic nodes of immune animals were more effective than cells from the mediastinal and mesenteric nodes. Immune spleen cells enhanced, rather than reduced, the degree of the infection. Cells or serum preparations from normal animals were not capable of transferring portective immunity to normal recipients.

Animals↗