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At least 937 records · Page 52Linked to original sources
PubMed2000

Anticancer drugs plus cytokines: immunodulation based therapies of mouse tumors.

As demonstrated in this laboratory, several cytotoxic anticancer agents have immunomodulating effects at relatively low doses and, in combination with non-toxic doses of certain cytokines, can exert immunity-dependent curative effects in mouse tumor models. Thus, adriamycin (Dox) has been shown to enhance the activation of macrophages with associated increases of IL1 and TNF production, to stimulate the production of IL2 and the development and action of CTLs. In the EL4 lymphoma C57BL/6 mouse model, combinations of appropriate regimens of Dox plus IL2 or TNF induce cures and the long-term survivors exhibit life-long immunological memory. Combinations of cyclophosphamide plus TNF have analogous effects. In the E0771 breast tumor C57BL/6 mouse model, Dox plus TNF at doses which are without antitumor activity when given alone, cause complete cures of established tumors with concomitant stimulation of CTL and NK cells responses. The mechanisms involved in these therapeutic responses are discussed. In conclusion, the results obtained substantiate the possibility of establishing antitumor curative combination regimens based on the utilization of low non-toxic immunomodulating doses of certain anticancer drugs and specific cytokines.

Adjuvants, Immunologic↗
PubMed1999

[Immunology of tuberculosis: current status].

The paper outlines the high-priority trends in basic and applied investigations of antituberculous immunity. It presents the results obtained from studies of the genetic mechanisms responsible for the control of susceptibility in experimental tuberculosis, from analyses of novel chemical and recombinant tuberculosis vaccines, from examinations of the role of immunological memory in the disease. While describing the results of tuberculosis immunodiagnosis, particular emphasis is laid on its major aspects: on the differential diagnosis of tuberculosis and other lung diseases and on the screening of high-risk group populations for disease progression in order to made further in-depth studies. Current aspects of evaluating the immune status and nonspecific responsiveness in patients with tuberculosis are considered.

Adjuvants, Immunologic↗
PubMed1996

Rapid induction of tumor necrosis factor cytotoxicity in naive splenic T cells by simultaneous CD80 (B7.1) and CD54 (ICAM-1) co-stimulation.

The co-expression of B7.1 (CD80) and intercellular adhesion molecule (ICAM)-1 (CD54) on tumor cells can induce tumor immunity and immunological memory. We show here that the non-immunogenic tumor lines Lewis lung carcinoma and B16F10 melanoma, co-transfected with B7.1 and ICAM-1, induced cytotoxic levels of membrane tumor necrosis factor (TNF) on naive syngeneic T cells within 24 h. Membrane TNF expression, primarily on CD4 cells, was responsible for tumor cell lysis by naive spleen cells and could be completely abolished by anti-TNF antiserum. It is suggested that the strong induction of TNF cytotoxicity may be important in the establishment of tumor immunity.

Animals↗
PubMed1987

Effect of dextran sulphate on IgG subclass of antibody in efferent popliteal lymph of sheep.

IgG1 and IgG2 participation in anti-hapten, anti-carrier and immunoglobulin-containing cell (Ig-cc) responses was studied in sheep immunised with killed Staphylococcus aureus-Dinitrophenyl (DNP) conjugates. The antigen was given with or without the polyanionic adjuvant dextran sulphate (DXS). Animals were immunised intracutaneously on the lateral hock of one hind leg with 1 X 10(9) S. aureus-DNP with or without 20 mg DXS. Six weeks later, primed sheep underwent surgery to cannulate an efferent popliteal lymphatic vessel in the immunised leg. Forty-eight hours after surgery, each sheep was given a further intracutaneous injection of 1 X 10(9) S. aureus-DNP with or without 20 mg DXS adjacent to the primary injection site. IgG1-cc and IgG2-cc in lymph were counted using indirect immunofluorescence. Total IgG1 and IgG2 anti-staphylococcal and anti-DNP antibody output in lymph was determined using enzyme-linked immunosorbent assays (ELISA's). DXS markedly increased antibody responses to S. aureus-DNP in the popliteal lymph node of sheep and was shown to strongly enhance immunological memory. The ratios of IgG2-cc:IgG1-cc and IgG2:IgG1 anti-staphylococcal antibody in lymph-draining popliteal lymph nodes of sheep stimulated with DXS and S. aureus-DNP was significantly greater than the same ratios in animals given antigen alone. The IgG subclass-specific immunomodulatory effects of DXS were exerted whether the adjuvant was given with primary and/or secondary inoculations. There was no difference in the ratio of IgG2:IgG1 anti-DNP antibody in lymph from animals given S. aureus-DNP with and without DXS.

Adjuvants, Immunologic↗
PubMed2004

IgG2a-mediated enhancement of antibody and T cell responses and its relation to inhibitory and activating Fc gamma receptors.

A number of studies in experimental animal models point to an important role of Fc gamma Rs in autoimmunity and allergy. In this study, we investigate how the production of IgG, an early step in the chain of events leading to inflammation, is regulated by activating and inhibitory Fc gamma Rs. IgG Abs are known to feedback-enhance Ab responses to soluble Ags, and this effect requires activating Fc gamma Rs. To test proliferation of Th cells, mice were adoptively transferred with CD4(+) T cells expressing a transgenic OVA-specific TCR before immunization with IgG2a anti-2,4,6-trinitrophenyl (TNP) plus OVA-TNP or with OVA-TNP alone. IgG2a induced a significant increase in OVA-specific T cell numbers, which preceded the OVA-specific Ab response and was dependent on the Fc gamma chain. The role of the inhibitory Fc gamma RIIB in Ab responses was studied in mice lacking this receptor. Although IgG2a enhanced primary Ab responses, development of germinal centers, and immunological memory in wild-type mice, enhancement was markedly stronger in Fc gamma RIIB(-/-) mice. The presented data are compatible with the hypothesis that the mechanism behind IgG2a-mediated up-regulation of Ab responses involves increased Ag presentation to CD4(+) T cells by Fc gamma R(+) APCs. Our observations also illustrate the intricate immunoregulatory role of IgG Abs. On the one hand, they enhance Ab responses via activating Fc gamma Rs, and on the other hand, they set an upper limit for the same Ab response via Fc gamma RIIB.

Adjuvants, Immunologic↗
PubMed1995

Vaccine adjuvants based on gamma inulin.

Algammulin and gamma-IN comprise a novel class of vaccine adjuvant. Their use in vaccines is to exploit the humoral defense known as the alternative pathway of complement. They use a "natural" mechanism and the biochemical basis of their action is well understood in general terms. They are fully researched up to the stage of specific commercial application. Inulin itself is registered for human use as a solution and is without physiological effect except for ACP activation as gamma-IN particles. The ACP comprises a relatively harmless part of the inflammatory response. Gamma inulin is nontoxic in several species including humans and is nonpyrogenic. The amount of systemic C3a produced from adjuvant-active doses of gamma-IN is expected to be very much less than that routinely tolerated without effect by human renal dialysis patients. Registration of gamma-IN should not be difficult. Gamma inulin in vivo is either dissolved and excreted unchanged or metabolized to simple foodstuffs. Its primary chemical structure is completely known, and it is inexpensive, readily available, and easy to handle and manufacture. It is completely stable under normal conditions of use and storage. Patent cover is either fully granted or accepted for granting in most developed countries. Alum is also registered for human use and its combination with gamma-IN known as Algammulin is equally nontoxic especially in the fine formulation, and is equally stable. The partial coating with inulin in Algammulin greatly reduces the undesirable effects of alum such as granuloma formation and IgE generation. Combinations of gamma-IN with immunogen carriers other than alum are feasible, either as hybrid particles or as simple mixtures of particles of similar size. Gamma inulin, and especially Algammulin, are potent enhancers of the Th1 immune response pathway, boosting seroconversion rates and immunological memory in protective Ab classes and enhancing cell-mediated immunity. The responses can equal those of CFA. They are also Th2 pathway enhancers, especially for IgA, and the emphasis on Th2 might be varied by altering the alum-to-inulin ratio in the final formulation. A dual response (balanced Th1 and Th2) may be desirable for several reasons. Their primary targets in vivo are probably lymphocytes rather than macrophages. Gamma inulin-based adjuvants therefore comprise new, safe, potent, and attractive candidates for enhancing responses to human and veterinary vaccines, especially those requiring cell-mediated defenses.

Adjuvants, Immunologic↗
PubMed2002

Mechanisms underlying UV-induced immune suppression: implications for sunscreen design.

The ultraviolet (UV) radiation present in sunlight is immune-suppressive. Recently we showed that solar-simulated UV radiation (UVA + UVB; 295-400 nm), applied after immunization, suppressed immunological memory and the elicitation of delayed-type hypersensitivity to the common opportunistic pathogen, Candida albicans. Further, we found that wavelengths in the UVA region of the solar spectrum (320-400 nm), devoid of UVB, were equally effective in activating immune suppression as UVA + UVB radiation. Here we report on the mechanisms involved. No immune suppression was found in UV-irradiated mice injected with monoclonal anti-interleukin (IL)-10 antibody, or mice exposed to solar-simulated UV radiation and injected with recombinant IL-12. Antigen-specific suppressor T cells were found in the spleens of mice exposed to UVA + UVB radiation. Applying liposomes containing bacteriophage T4N5 to the skin of mice exposed to solar-simulated UVA + UVB radiation or mice exposed to UVA radiation blocked immune suppression, demonstrating an essential role for UV-induced DNA damage in the suppression of established immune reactions. These findings indicate that UV radiation activates similar immunological pathways to suppress the induction, or the elicitation, of the immune response.

Animals↗
PubMed1989

T cells in transplantation immunity.

This paper reviews the following problems in transplantation immunity: (i) short-lived ability to transfer immunity or suppression, in contrast to long-lived immunological memory in the autochthonous animal; (ii) short-lived ability to transfer graft-resistance, in contrast to long-lived ability to transfer helper activity for B-cells; (iii) the response to H-Y, as a system that might solve some outstanding problems in antigen presentation; and (iv) the contrast between live and killed allogeneic cells as immunogens. All of these problems, it is suggested, are amenable to study by modern methods. Students like me were drawn into Peter Medawar's orbit in the 1940s and 1950s by an irresistible mix of intellectual challenge and the glamour of experimental surgery. Much the same was happening elsewhere in the laboratories of Ray Owen, Milan Hasek, George Snell, Burnet, and Florey, and by 1960 the transplantation immunologists could justly claim to have opened up a whole new area of ideas in biology: we had discovered the lymphocyte as the antigen-sensitive cell, and the principles of immunological tolerance; we had revived interest in cellular immunity, and it was we who found the MHC (even if we had little idea of its real meaning). But by 1960 the first wave of success had passed, and the penetration of immunology by molecular biology had begun. Interest in transplantation immunity perceptibly declined, although many groups continued to address important problems, particularly in the field of organ transplantation. (ABSTRACT TRUNCATED AT 250 WORDS)

Graft Rejection↗
PubMed2001

Enhancing cytotoxic T cell responses with altered-peptide ligands.

Interest in class I MHC-mediated immunotherapy is growing rapidly. In order to fight a virus or cancer effectively, a successful immunotherapeutic must activate a large number of specific CD8+ T cells and also generate immunological memory. Attempts to generate immune responses towards tumor- or virus-derived peptides have frequently been frustrated by the nature of the peptide antigen itself. Either the peptide does not bind well to its cognate MHC, or the T cells directed towards it have been functionally inactivated in vivo. Altered-peptide ligands (APL) are an effective way to circumvent these problems. However, generating enhanced binding of altered peptides to class I MHC while still maintaining recognition of the wild-type peptide is not straightforward. Many groups design enhanced binding peptides by substituting the observed anchor residues with those that are most preferred by the class I MHC molecule. For many antigenic peptides, this approach does not work. Furthermore, if a higher affinity peptide is designed, the substitutions may result in reduced recognition by CD8+ T cells. Therefore, the design of APL requires careful testing of each candidate therapeutic in terms of affinity for class I MHC and immunological reactivity. Lastly, immunotherapy using class I MHC must also take into account the large genetic heterogeneity in the population. A therapeutic that is only effective for 5-10% of the population is not as attractive as one that works for over 90% of the population. The use of MHC supertypes (groups of class I MHC allotypes that share similar peptide-binding characteristics) shows great promise in overcoming this problem.

Amino Acid Sequence↗
PubMed1986

Potential uses of interleukin 2 in cancer therapy.

Interleukin 2 (IL 2) has several potential uses in cancer therapy including: the augmentation of specific T cell mediated anti-tumor immunity and the activation of non-specific cytolytic effector cells, termed lymphokine-activated killer (LAK) cells. The current review will present data from our laboratory demonstrating in animal models the feasibility of both potential approaches. Studies to be reviewed show that: IL 2 can induce the proliferation and expansion in number of tumor-reactive T cells in vitro; T cells grown in culture in IL 2 can be effective reagents in vivo for specific tumor therapy; the administration of exogenous IL 2 can induce the growth and augment the function of cultured T cells in vivo; however, as a corollary, T cells cultured long-term in vivo with IL 2 are functionally limited in vivo without the administration of exogenous IL 2 in vivo; by contrast, T cells grown in vitro with specific antigen, as opposed to IL 2, as the major stimulus for proliferation are able to proliferate rapidly in vivo, distribute widely in host lymphoid organs, and mediate therapy of disseminated murine leukemia; importantly, such antigen-driven long-term cultured T cells can survive long-term in vivo and provide specific immunologic memory, and, the administration of low-dose IL 2 in vivo can induce the growth of antigen-driven long-term cultured T cells in vivo and thereby increase the number of functional memory T cells; the culture of lymphoid cells in high concentrations of IL 2 can induce LAK cells in vitro capable of lysing leukemia in vitro; LAK cells generated in vitro can mediate a small but detectable anti-tumor effect in vivo against disseminated leukemia as an adjunct to chemotherapy; and, high-dose IL 2 administered in vivo can activate LAK cells in vivo and cure disseminated murine leukemia. Therefore, it is highly likely that IL 2 can become an effective reagent for the therapy of human cancer.

Animals↗
PubMed1993

The role of T-helper lymphocytes in priming for experimental autoimmune glomerulonephritis in the BN rat.

In our model of experimental autoimmune glomerulonephritis (EAG), BN rats given a single IM injection of homologous glomerular basement membrane (GBM) in FCA develop anti-GBM autoantibodies with focal glomerulonephritis. To investigate the role of lymphocytes in the induction of EAG, we examined the effects of antigen rechallenge and of adoptive cell transfer from donors with nephritis to naive recipients. Groups of animals were rechallenged with GBM in FCA following either low (non-nephritogenic) doses of GBM, or following resolution of EAG. This resulted in an enhanced anti-GBM antibody response in both groups, suggesting the presence of GBM specific T or B memory cells. To investigate this possibility, spleen cells from animals with EAG were transferred into lightly irradiated recipients. There was no significant rise in anti-GBM antibody levels after transfer. However, subsequent challenge with GBM in FCA resulted in an enhanced anti-GBM antibody response by 2 weeks when compared with recipients of normal spleen cells. Cells capable of priming for EAG developed by week 4 after immunization of donors and persisted in the recipients for at least 24 weeks. To investigate which cell type was responsible for this effect, we depleted or positively selected donor spleen cells prior to transfer, using Dynabeads coated with monoclonal antibodies to Th or B lymphocytes. Depletion of Th cells, but not B cells, reduced the enhanced anti-GBM antibody response of recipients challenged with GBM in FCA. Positively selected Th cells, but not B cells, resulted in an enhanced anti-GBM antibody response similar to that in positive controls. These results demonstrate the presence of immunological memory for the autoantigen and show that priming for EAG is mediated by Th lymphocytes.

Animals↗
PubMed1983

Parenteral immunization causes antigen-specific cell-mediated suppression of an intestinal IgA response.

Rats immunized s.c. with cholera toxin (CT) or toxoid (CTd) show antigen-specific suppression of the jejunal IgA anti-CT response to subsequent enteric doses of CT. We determined whether this effect was partly cell-mediated and studied the suppressor cell response involved. Spleen cells from s.c.-immunized rats suppressed the jejunal anti-CT response in adoptive recipients when cell transfer was at, or 4 days before, intraduodenal priming with CT. Transferred suppression was antigen-specific, and the suppressor cells were nylon wool-nonadherent. Increasing the s.c. dose of CT from 0.1 to 40 micrograms, and the interval between immunization and cell harvest from 2 to 16 wk, each increased the suppressive effect of a constant spleen cell inoculum. After s.c. immunization, suppressor cells were present in the spleen within 1 to 2 wk, among TDL within 4 to 8 wk, and in Peyer's patches and thymus within 8 to 16 wk; this sequence suggested they arose in the spleen and later migrated to mucosae and the thymus. Prior splenectomy did not alter the suppressive effect of s.c. CT, however, nor did it prevent suppressor cell appearance among TDL, indicating that suppressor cells also arose from nonsplenic sites. Transferred suppressor cells acted by interfering with the development of specific immunologic memory within Peyer's patches during enteric priming; transfer of suppressor cells at the time of enteric boosting had no effect upon the secondary mucosal anti-CT response. We conclude that the suppressive effect of s.c. immunization on a specific mucosal IgA response is due largely to the action of systemically derived suppressor cells upon the primary mucosal immune response within Peyer's patches. This sequence resembles the mirror image of oral tolerance, which involves the suppression of systemic IgG and IgM responses by suppressor cells that arise in Peyer's patches and migrate to the spleen after antigen feeding.

Animals↗
PubMed2001

Vehicles for genetic vaccines against human immunodeficiency virus: induction of T cell-mediated immune responses.

Success of a candidate vaccine against human immunodeficiency virus (HIV) depends on the type, site, strength, longevity and specificity of the immune responses it induces. The specificity of a vaccine is determined by the HIV-derived immunogens it employs in its formulation. Central to the other features is a correct and efficient delivery of the immunogens to the relevant cells of the immune system, which leads to orchestrated actions of millions of cells of several types and functions at multiple sites in the body. Thus, for elicitation of cytotoxic T lymphocyte responses, immunogens have to be delivered to the so called 'professional' antigen-presenting cells in a way that leads to a specific activation and expansion of naïve or precursor T cells, subsequent maturation of effector functions and, importantly, generation of a potent immunological memory. Many aspects of theseprocesses are currently unknown. However, it is very likely that the immunogenicities of genetic vaccines, i.e. vaccines delivering genes coding for immunogens rather than purified possibly adjuvanted proteins or peptides themselves, are in great part determined by the choice of vaccine vehicles and route of administration. In addition, vaccine immunogenicities can be augmented semi-rationally by immunogen engineering and co-delivering immunomodulatory molecules, and empirically by combining different vehicles expressing the same immunogen in heterologous prime-boost protocols. In any case, a successful vaccination strategy against HIV as well as other chronic viral infections has to elicit better immune responses than the natural infections do.

AIDS Vaccines↗
PubMed1994

Immunotherapy of prostate cancer in the Dunning rat model: use of cytokine gene modified tumor vaccines.

Adenocarcinoma of the prostate is the most common cancer in men. The majority of cancers are discovered once they have already metastasized, and there is no effective therapy for prostatic cancer at this stage. The use of cytokine-secreting tumor cell preparations as therapeutic vaccines for the treatment of advanced prostate cancer was investigated in the Dunning rat R3327-MatLyLu prostatic tumor model. IL-2 secreting, irradiated, tumor cell preparations were capable of curing animals with s.c. established tumors, and induced immunological memory that protected animals from subsequent tumor challenge. Immunotherapy was less effective when tumors were induced orthotopically, but nevertheless led to improved outcome, significantly delaying, and occasionally preventing, recurrence of tumors after resection of the cancerous prostate. Granulocyte-macrophage colony stimulating factor secreting tumor cell preparations were less effective, and interferon-gamma secreting cells had only a marginal effect. Induction of a potent immune response in tumor bearing animals against the nonimmunogenic MatLyLu tumor supports the view that active immunotherapy warrants further investigation as a potential therapeutic approach to prostate cancer.

Adenocarcinoma↗
PubMed1999

Presence of effector CD8+ T cells in hepatitis C virus-exposed healthy seronegative donors.

CTL responses against multiple hepatitis C virus (HCV) epitopes were detected in 7 of 29 (24.1%) healthy family members (HFM) persistently exposed to chronically HCV-infected patients (HCV-HFM). These precursor CTL were at very low or undetectable frequencies, as determined by limiting dilution analysis. However, when HCV-specific effector CD8+ T cells, freshly isolated from PBMC of HCV-HFM, were assessed by a sensitive enzyme-linked immunospot assay, their frequencies were severalfold higher than those of precursor CTL. These results indicate that the two assays detect two functionally distinct T cell populations and that the effector cells are not assayed by the 51Cr-release assay. Furthermore, the combination of cell depletion and enzyme-linked immunospot analyses showed that the effector cells were confined into a CD8+ CD45RO+ CD28- population. The persistence of effector CD8+ T cells specific for both the structural and nonstructural viral proteins in uninfected HCV-HFM, suggest that: 1) an immunological memory is established upon a subclinical infection without any evidence of hepatitis, in a large cohort of HCV-exposed individuals; 2) because these cells required neither restimulation nor the addition of particular cytokines in vitro for differentiating in effectors, they should be capable of prompt HCV-specific effector function in vivo, possibly providing antiviral protection; and 3) the maintenance of effector T cell responses may be sustained by persisting low-level stimulation induced by inapparent infections.

Adolescent↗
PubMed1979

Surface markers on natural killer cells of the mouse.

Rabbit antiserum against mouse brain tissue (anti-brain-associated T cell antigen, anti-BAT) was capable of killing splenic natural killer (NK) cells of CBA/J, BALB/c, C 57 Bl/6J, C 3 H/He and nude mice, which were detected with Molony virus-induced lymphoma (YAC-1) and radiation-induced leukemia (RL male 1) cells as targets. The same antiserum abolished T cell functions, e.g. carrier-specific helper function and the responsiveness to concanavalin A, but not B cell functions, e.g. immunological memory for the secondary antibody response and the responsiveness to lipopolysaccharide. After absorption of the anti-BAT with thymocytes, the ability to kill T cells was completely abrogated, leaving the activity to kill NK cells intact. No other heterologous and isologous antisera, i.e. rabbit anti-mouse thymocyte antiserum, goat antiserum against antigens shared by thymus and B cells, anti-Thy-1.2 and anti-Ia antisera, could eliminate NK function regardless of their definite reactivity against T or B cells. The results indicate that the absorbed anti-BAT can distinguish NK cells from other known subsets of T and B cells.

Animals↗
PubMed2004

Dose response of CRM197 and tetanus toxoid-conjugated Haemophilus influenzae type b vaccines.

High vaccine cost has limited use of conjugate vaccines in the developing world where the disease burden is greatest. Fixed fractional doses of Haemophilus influenzae type b (Hib) vaccines have been shown to be immunogenic, but dose responses of these vaccines in humans are needed to determine the lowest immunogenic dose as an option for lowering vaccine cost. We randomized children to receive one of five doses (0.625, 1.25, 2.5, 5.0 and 10 microg) of either a diphtheria CRM197 or tetanus toxoid-conjugated Hib vaccine. The children received a primary three-dose series at 6, 10, and 14 weeks of age and a booster dose at 9 months. Anti-PRP IgG antibodies were measured at each vaccination, at 18 weeks, and at one week following the booster dose. Concentrations of > or =1.25 microg of HibCRM197 vaccine produced mean anti-PRP responses at 18 weeks of > or =5.72 microg/ml and > or =0.15 microg/ml was achieved in >98% of the children with at least 79% reaching anti-PRP concentrations of > or =1.0 microg/ml. Concentrations of > or =1.25 microg of Hib-tetanus vaccine produced mean anti-PRP responses at 18 weeks of > or =8.63 microg/ml and > or =0.15 microg/ml was achieved in 100% of the children with at least 88.9% reaching anti-PRP concentrations of > or =1.0 microg/ml. While mean antibody concentrations after either vaccine decreased over time, the proportion of children with antibody levels of > or =0.15 microg/ml had not changed significantly at the 9 month measurement. Immunologic memory was demonstrated by significant increases in mean antibody concentrations one week after the booster dose for doses > or =1.25 microg of HibCRM197 and Hib-tetanus to mean concentrations > or =37.71 and 16.07 microg/ml, respectively. There were no differences in antibody responses for vaccine doses > or =1.25 microg of the same vaccine or between the same concentrations of the two different vaccines. Our data suggest that doses of these vaccines of > or =1.25 microg may be sufficient to stimulate an immune response that offers both short and longer term protection from invasive Hib disease.

Diphtheria-Tetanus-Pertussis Vaccine↗
PubMed2006

Autophagy and antigen presentation.

CD4(+) T cells co-ordinate adaptive immunity and are required for immunological memory establishment and maintenance. They are thought to primarily recognize extracellular antigens, which are endocytosed, processed by lysosomal proteases and then presented on major histocompatibility complex (MHC) class II. However, recent studies have demonstrated that viral, tumour and autoantigens can gain access to this antigen presentation pathway from within cells by autophagy. This review will discuss the autophagic pathways that contribute to endogenous MHC class II antigen processing. Furthermore, potential characteristics of autophagy substrates, qualifying them to access these pathways, and regulation of autophagy will be considered. Finally, I will suggest how antigen presentation after autophagy might contribute to immune surveillance of infected and transformed cells.

Animals↗