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PubMed1986

[Protein deficiency, host defense and natural anti-tumor immunity].

Natural immuneffector cells, namely natural killer cells and monocyte/macrophages, have become in recent years an important part of theory and practice of immunotherapy. This is especially the case for therapy of malignant tumors with biological response modifiers (BRMs). Many BRMs increase cytotoxicity against tumor cells and cell numbers of natural immuneffector cells. Protein depletion on the other hand, which often is part of malignant diseases, results in well known negative effects on acquired and specific immunity. The data which are presented here show that depressions of natural immuneffector cells in terms of cytotoxicity and cell numbers also occur after protein depletion. The same is true for their pool, the bone marrow. The potentials of BRM therapy are considerably decreased. Host defense mechanisms in normal and protein depleted nutritional status, immunological tumor defense and BRM therapy are presented in the survey.

Adjuvants, Immunologic↗
PubMed2005

[Mechanisms of innate immunity].

Innate (natural) immunity differs from acquired immunity with respect to the detection systems (receptors and structures detected on pathogens), the cells engaged, and the nature of the mechanisms. Innate immunity is an ancient system, with similar structures in plants, invertebrates, and vertebrates are involved in the development of defense against pathogens. Toll-like receptor (TLR) structures are present in all organisms, and some mechanisms (i.e. complement activation) were also discovered in invertebrates and vertebrates. During infection, innate reactions develop before acquired immune reactions do. Natural immunity involves such reactions as the production of different cytokines, chemokines, and interleukins; the innate, cytokines-dependent nonspecific immunity of leukocytes; HLA-independent pathogen-killing cells, and phagocytosis. Such cytokines as interferons, the TNF family, and interleukines 12 and 18 participate in antiviral, antibacterial, antiprotozoan and anticancer natural immunity. NK cells, cytokines of the TNF family, and the complement system activated by lectins are engaged in the non-specific killing of infected or tumor cells. As over-activation of the innate system can be dangerous, the system must be submitted the strict control. The exact mechanism of this control system is not yet known, but there are several indications of its presence.

Animals↗
PubMed1997

Physical exercise, endogenous opioids and immune function.

The experimental data available today strongly indicate that various types of physiological stressors, including physical exercise and emotional stress, can influence immune function. Natural immunity represents a first line of defence in viral infections and cytotoxicity to a variety of tumour cells. Natural immunity is strongly influenced by chronic exercise and this regulation includes interaction between the nervous, endocrine and immune systems. Central mechanisms including the endogenous opioids are of great interest. Chronic activation of endogenous opioid systems augments natural cytotoxicity and the possible involvement the opioids in the exercise-induced enhancement of natural immunity is discussed. Also, catecholamines seem to play an important role in the regulation of immune function, both after chronic exercise and emotional stress. The physiological significance of the reported changes in natural cytotoxicity after exercise-training is as yet unclear.

Animals↗
PubMed1984

'Naturally occurring' anti-D in Rh(D) negative volunteers for immunization.

'Naturally occurring' anti-D has been studied in four Rh(D) negative males. The presence of this anti-D does not preclude successful deliberate immunization of Rh(D) negative volunteers; 'naturally occurring' anti-D does not provide a marker of non-responders to Rh immunization. 'Naturally occurring' anti-D is not necessarily the result of materno-fetal transfusion at birth.

Humans↗
PubMed1988

Modulation of human malaria transmission by anti-gamete transmission blocking immunity.

Natural Plasmodium vivax malaria infections in man evoke anti-gamete transmission blocking antibodies which influence the infectivity of malaria patients to the vector mosquito. In this study, entomological, immunological and parasitological data obtained through the monitoring of an epidemic of human vivax malaria in Sri Lanka were used in a mathematical simulation to assess the effect of naturally induced transmission blocking immunity on malaria transmission. A mathematical model to describe malaria transmission accounting for transmission blocking immunity was developed from the basic differential equations originally stated by R. Ross and the epidemic was simulated using the available data. An attempt was made to predict the monthly malaria incidence by means of the mathematical simulation, with and without accounting for transmission blocking immunity. A plausible mathematical solution of the epidemic could be obtained when transmission blocking immunity was accounted for, and it was not possible to obtain such a plausible solution in the absence of immunity. Thus, the postulated occurrence of transmission blocking immunity was essential to describe adequately this malaria epidemic, indicating that, at least in epidemic situations, naturally occurring transmission blocking immunity has a controlling influence on malaria incidence.

Animals↗
PubMed2000

Natural antibodies and complement link innate and acquired immunity.

Natural or spontaneous antibodies are an essential part of the first line of defense against hematogenically spreading infections, including viruses. These antibodies target virus-antibody complexes and complement to the spleen. This prevents infections from reaching vital organs and enhances neutralizing antibody responses, particularly when the antibody is bound to a highly repetitive antigen.

Animals↗
PubMed2002

Natural killer T (NKT) cells and their role in antitumor immunity.

Natural killer T (NKT) cells have become a major focus for those who study the innate immune response to tumors and infectious diseases, as well as autoimmunity. These novel T lymphocytes produce both Th1 and Th2 cytokines, recognize phospholipid and glycolipid antigens presented by CD1 molecules in a similar manner as peptides are recognized by cytotoxic T lymphocytes (CTL), and kill tumor cell targets by a perforin-dependent mechanism like NK cells and CTL. These ascribed functions thus demonstrate that NKT cells are a unique cytotoxic effector cell subpopulation with a kaleidoscope of activities. Because they can mediate antitumor effects in vivo with or without the collaboration of NK cells, the study of NKT cells in antitumor immunity may lead to novel treatments based on the ability to manipulate the generation and/or activity of these multifunctional lymphocytes.

Antigens, CD1↗
PubMed2005

Naturally arising CD25+CD4+ regulatory T cells in tumor immunity.

Naturally arising regulatory T (TR) cells, represented by CD25+CD4+ TR cells, play an essential role in maintaining immunological self-tolerance. This T cell-mediated dominant control of the immune response not only inhibits the development of autoimmune disease, but also impedes effective immunosurveillance against autologous tumor cells. Attenuation of TR cell-mediated immune suppression can therefore evoke effective tumor immunity in otherwise nonresponsive animals. This common regulatory mechanism for autoimmunity and tumor immunity can be exploited when devising a novel immunotherapy for cancer.

Animals↗
PubMed2005

Natural killer cells in hepatitis C virus infection: from innate immunity to adaptive immunity.

Natural killer (NK) cells are specialized lymphocytes that provide a first line of defense through their ability to kill pathogen-infected cells and transformed cells. The function of NK cells is regulated by a fine balance of inhibitory and activating signals, which are mediated by a diverse array of cell-surface receptors. We recently found that expression of the inhibitory receptor CD94/NKG2A is up-regulated on NK cells in patients with chronic hepatitis C. HLA-E, a ligand for NKG2A, was expressed in all human hepatoma cell lines tested as well as in nontransformed hepatocytes, but not in K562 cells, a classic NK-sensitive target. NK cells isolated from patients with chronic hepatitis C (HCV-NK) were less capable of killing hepatoma cells and of producing interferon-gamma in response to hepatoma cells than those from healthy donors, whereas there was no significant difference in NK responsiveness toward K562 cells. Of note is the finding that maturation and activation of monocyte-derived dendritic cells were negatively modulated in the presence of HCV-NK and hepatoma cells, which were restored by the addition of anti-NKG2A antibody during the coculture of HCV-NK and hepatoma cells. Research revealed that dendritic cells recognize danger signals from microorganisms by monitoring pathogen-associated molecular patterns via Toll-like receptors. Our findings have shed light on NK receptors as an important interface that transmits danger signals from abnormal cells to immune systems. Aberrant expression of CD94/NKG2A should have negative impact on innate resistance and subsequent adaptive immunity toward HCV-infected or transformed cells in chronic hepatitis C.

Cell Communication↗
PubMed2005

The role of natural killer cells in tumor control--effectors and regulators of adaptive immunity.

Natural killer (NK) cells are the primary effector cells of the innate immune system and have a well-established role in tumor rejection in a variety of spontaneous and induced cancer models. NK cell function is regulated by a complex balance of inhibitory and activating signals that allow them to selectively target and kill cells that display an abnormal pattern of cell surface molecules, while leaving normal healthy cells unharmed. In this review we discuss NK cell function, the role of NK cells in cancer therapies, the emerging concept of bi-directional cross-talk between NK cells and dendritic cells, and the implications of these interactions for tumor immunotherapy.

Animals↗