Leukocyte and Lymphocyte: Acute Radiation Cytotoxicity.DMITRI POPOV MEDICAL DOCTOR ( RUSSIA)PHD, RADIOBIOLOGY. ADVANCED MEDICAL TECHNOLOGY AND SYSTEMS. (CANADA).

Leukocyte and Lymphocyte

The complicated story about two brothers - Lymphocyte and Leukocyte, and their terrible relationships with their Uncle Radiation.

Leukocyte and Lymphocyte

Implications for immune-prophylaxis and immune-therapy of Acute Radiation Disease.

Leukocyte and Lymphocyte.

White blood cells (WBCs), also called leukocytes  are the cells of the immune system that are involved in protecting the body against both infectious disease and foreign invaders or physical factors or cancer. All leukocytes are produced and derived from a multipotent cell in the bone marrow known as a hematopoietic stem cell. Leukocytes are found throughout the body, including the blood and lymphatic system.

White cells are best classified into two major line-ages: the myeloid leukocytes and the lymphocytes.

Maton, D., Hopkins, J., McLaughlin, Ch. W., Johnson, S., Warner, M. Q., LaHart, D., & Wright, J. D., Deep V. Kulkarni (1997). Human Biology and Health. Englewood Cliffs, New Jersey, US: Prentice Hall. ISBN 0-13-981176-1.

Leukocyte and Lymphocyte: Acute Radiation Cytotoxicity.

Polymorphonuclear leukocyte - A type of immune cell that has granules (small particles) with enzymes that are released during Radiation, infections, allergic reactions, and asthma. Neutrophils, eosinophils, and basophils are polymorphonuclear leukocytes. A polymorphonuclear leukocyte is a type of white blood cell.

Also called granular leukocyte, granulocyte, and PMN. http://www.cancer.gov/publications/dictionaries/cancer-terms?

cdrid=633963

Leukocyte and Lymphocyte.

Polymorphonuclear Leukocytes are one of the main sources of enzymes.

Enzymes responsible for tissue damages and inflammation development. Baggiolini et al. 1978.

Eight acid hydrolases, peroxidase (EC 1.11.1.7), cyanide-insensitive NADH oxidase and alkaline phosphatase (EC 3.1.3.1.) were demonstrated in homogenates of human polymorphonuclear leukocytes. Studies on human polymorphonuclear leukocyte enzymes. I. Assay of acid hydrolases and other enzymes

JoséLuis Avila,  Jacinto Convit

Leukocyte and Lymphocyte.

A low-molecular-weight component of complement, similar to or identical with human C5a, interacts with human polymorphonuclear leukocytes treated with cytochalasin B and provokes extracellular release of lysosomal enzymes from these cells. Enzyme release occurs in the absence of particles and is selective in that it is not accompanied by release of cytoplasmic enzymes. Ultrastructural histochemistry of cells exposed to this component of complement revealed degranulation, fusion of lysosomal with plasma membranes, and transient assembly of microtubules associated with the release of endogenous myeloperoxidase. This intracellular events are common to two important responses of polymorphonuclear leukocytes in inflammation and tissue injury: (a) release of lysosomal hydrolases and (b) chemotaxis. < Mechanisms of Lysosomal Enzyme Release from Human Leukocytes: Microtubule Assembly and Membrane Fusion Induced by a Component of Complement . > Goldstain I. Proc. Nat. Acad. Sci. USA Vol. 70, No. 10, pp. 2916-2920, October 1973 .

Leukocyte and Lymphocyte.

The distribution of peroxidase and six lysosomal enzymes (acid phosphatase, arylsulfatase, beta-galactosidase, beta-glucuronidase, esterase, and 5'-nucleotidase) corresponded to that of azurophil granules. J Cell Biol. 1968 Nov;39(2):286-98. Differences in enzyme content of azurophil and specific

granules of polymorphonuclear leukocytes. I. Histochemical staining of bone marrow smears.

Bainton DF, Farquhar MG.

Leukocyte and Lymphocyte.

Polymorphonuclear leukocytes of rabbits and chickens after homogenization in 0.34 M saccharose or after multiple freezing and thawing were subjected to differential centrifugation at 150, 800, 10 000 and 50 000 X g. In the fractions obtained in this manner, total bactericidal activity as well as the activity of myeloperoxidase (E.C. 1. 11. 1. 7), catalase (E.C. 1.11.1.6), lysozyme (E.C. 3.2.1.17), cathepsin D (E.C. 3.4.4.23) and E, beta-D-glucuronidase (E.C. 3.2.1.31) and acid phosphatase (E.C. 3.1.3.2) were determined.

J Hyg Epidemiol Microbiol Immunol. 1976;20(1):91-100. Localization of antibacterial activity and hydrolytic enzymes in

subcellular fractions of rabbit and chicken Polymorphonuclear leukocytes.

Ferencĭk M, Stefanovic J, Absolonová O, Kotulová D.

Leukocyte and Lymphocyte.

Antibacterial activity was found in all fractions from rabbit leukocytes, but only in the first fraction from chick leukocytes. The fractions from rabbit leukocytes contained all enzymes under study while in the fractions from chicken leukocytes the presence of myeloperoxidase, catalase or cathepsin E could not be demonstrated. The highest bactericidal activity was found in the second obtained from the homogenate or rabbit leukocytes.

J Hyg Epidemiol Microbiol Immunol. 1976;20(1):91-100. Localization of antibacterial activity and hydrolytic

enzymes in subcellular fractions of rabbit and chicken Polymorphonuclear leukocytes.

Ferencĭk M, Stefanovic J, Absolonová O, Kotulová D.

Leukocyte and Lymphocyte.

The highest specific activity of myeloperoxidase and homogenate of rabbit leukocytes. The highest specific activity of myeloperoxidase and the lowest activity of cathepsin D were also demonstrated in this fraction. The addition of pepstatin to rabbit leukocytes before their disintegration resulted in the inhibition of the activity of cathepsin D and E and in an increase in the specific activity of myeloperoxidase as well as in total bactericidal activity in the individual fractions.

J Hyg Epidemiol Microbiol Immunol. 1976;20(1):91-100. Localization of antibacterial activity and hydrolytic enzymes

in subcellular fractions of rabbit and chicken Polymorphonuclear leukocytes.

Ferencĭk M, Stefanovic J, Absolonová O, Kotulová D.

Leukocyte and Lymphocyte.

Phagocytic leukocytes consume oxygen and generate reactive oxygen species in response to appropriate stimuli. The phagocyte NADPH oxidase, a multiprotein complex, existing in the dissociated state in resting cells becomes assembled into the functional oxidase complex upon stimulation and then generates superoxide anions.

Reactive oxygen species in phagocytic leukocytes John M. Robinson Histochem Cell Biol (2008) 130:281–297 DOI 10.1007/s00418-

008-0461-4.

Leukocyte and Lymphocyte.

The respiratory burst is mediated by the NADPH-oxidase complex, a multicomponent system that is rapidly assembled following activation of neutrophils. As we have discussed previously, the neutrophil NADPH oxidase produces O2 - and hydrogen peroxide (H2O2) following activation (Robinson et al. 2004).

Leukocyte and Lymphocyte.

Both H2O2 and O2 - are components of the oxygen-dependent, antimicrobial system of phagocytic leukocytes (e.g., Robinson and Badwey 1995).

The cytotoxic effects of O2 - and H2O2 relate to their ability to react with products of other microbicidal systems or autoimmune reeactions in these cells to generate additional reactive oxygen species (ROS) [e.g., hydroxyl radical (OH), singlet oxygen , ozone .

Superoxide can react with either hypochlorous acid (HOCl) or nitric oxide (NO) to produce OH

(Beckman et al. 1990; Ramos et al. 1992).

Leukocyte and Lymphocyte.

Hypochlorous acid and nitric oxide are produced in phagocytic leukocytes by myeloperoxidase and nitric oxide synthase, respectively (Harrison and Schultz 1976; Xie et al. 1992).

Singlet oxygen can form by non enzymatic dismutation of superoxide (Corey et al. 1987).

Reactive oxygen species in phagocytic leukocytes John M. Robinson

Leukocyte and Lymphocyte.

Highly enriched bovine polymorphonuclear neutrophils (PMN) were able to destroy herpesvirus-infected cells in the presence of complement. Our results suggest that some viral antigens are capable of activating the alternate complement pathway directly which results in cytotoxicity however, the addition of PMN plus complement resulted in high levels of cytotoxicity.

Leukocyte and Lymphocyte.

The PMN actively secretes cytolytic substances (Henney, 1975; Sellin, Wallch & Fischer, 1971) or just allows rearrangement of the target cell membrane as has been proposed for ADCC and antibodycomplement mediated lysis (Clark & Klebanoff, 1977; Juy, Billecocq, Faure & Bona, 1977; Mayer, 1977; Grewal et al., 1980) remains to be determined.

Leukocyte and Lymphocyte.

The evidence from our experiments would appear to suggest the latter since cell-free supernatants from the cultures were inactive in CDNC and secondly direct contact between the PMN and target cell was required for cytotoxicity to occur.

Immunology 198040 151 Complement-dependent, polymorphonuclear neutrophil-

mediated cytotoxicity of herpesvirus-infected cells: possible mechanism(s) ofcytotoxicity

A. S. GREWAL & L. A. BABIUK Department ofVeterinary Microbiology, Western CollegeofVeterinary Medicine, University ofSaskatchewan, Saskatoon, Canada

Leukocyte and Lymphocyte.

Mature natural killer (NK) cells use Ca 2 + -dependent granule exocytosis and release of cytotoxic proteins, Fas ligand (FasL), and membrane-bound or secreted cytokines (tumor necrosis factor [TNF] a ) to induce target cell death. Fas belongs to the TNF receptor family of molecules, containing a conserved intracytoplasmic “death domain” that indirectly activates the caspase enzymatic cascade and ultimately apoptotic mechanisms in numerous cell types. Two additional members of this family, DR4 and DR5, transduce apoptotic signals upon binding soluble TNF-related apoptosis-inducing ligand (TRAIL) that, like FasL, belongs to the growing TNF family of molecules.

Natural Killer (NK) Cell–mediated Cytotoxicity: Differential Use of TRAIL and Fas Ligand by Immature and Mature Primary Human NK Cells By Loris Zamai, Manzoor Ahmad, Ian M. Bennett, Livio Azzoni, Emad S. Alnemri, and Bice Perussia

From the Jefferson Medical College, Department of Microbiology and Immunology, Kimmel Cancer Institute, Philadelphia, Pennsylvania 19107

Leukocyte and Lymphocyte.

Unseparated peripheral blood leukocytes obtained from patients with rheumatoid arthritis (RA) were cytotoxic for synovial cells. The cytotoxic reactions produced by RA leukocytes were more frequent and of greater magnitude than cytotoxicity induced by leukocytes from normal persons and patients with other diseases, primarily connective tissue diseases.

The Cytotoxicity of Leukocytes and Lymphocytes from Patients with Rheumatoid Arthritis for Synovial Cells DoNALD A. PERSON, JoH T. SHAP, and MAIRN D. LIDSKY From the Departments of Internal Medicine and Virology and

Epidemiology, Baylor College of Medicine, Houston, Texas 77030

Leukocyte and Lymphocyte.

The human leukocyte antigen (HLA) system is the locus of genes that encode for proteins on the surface of cells that are responsible for regulation of the immune system in humans.The HLA genes are the human versions of the major histocompatibility complex (MHC) genes that are found in most vertebrates (and thus are the most studied of the MHC genes.

Leukocyte and Lymphocyte.

HLAs corresponding to MHC class I (A, B, and C) present peptides from inside the cell. For example, if the cell is infected by a virus, the HLA system brings fragments of the virus to the surface of the cell so that the cell can be destroyed by the immune system. These peptides are produced from digested proteins that are broken down in the proteasomes. In general, these particular peptides are smallpolymers, about 9 amino acids in length.[citation needed] Foreign antigens presented by MHC class I attract killer T-cells (also called CD8positive- or cytotoxic T-cells) that destroy cells.

HLAs corresponding to MHC class II (DP, DM, DOA, DOB, DQ, and DR) present antigens from outside of the cell to T-lymphocytes. These particular antigens stimulate the multiplication of T-helper cells, which in turn stimulate antibody-producing B-cells to produce antibodies to that specific antigen. Self-antigens are suppressed by regulatory T cells.

HLAs corresponding to MHC class III encode components of the complement system.

Leukocyte and Lymphocyte.

When a foreign pathogen enters the body, specific cells called antigen-presenting cells (APCs) engulf the pathogen through a process called phagocytosis. Proteins from the pathogen are digested into small pieces (peptides) and loaded onto HLA antigens (to be specific, MHC class II). They are then displayed by the antigen-presenting cells to T cells, which then produce a variety of effects to eliminate the pathogen.

Through a similar process, proteins (both native and foreign, such as the proteins of virus) produced inside most cells are displayed on HLAs (to be specific, MHC class I) on the cell surface. Infected cells can be recognized and destroyed by CD8+ T cells.

Leukocyte and Lymphocyte.

Any cell displaying some other HLA type is "non-self" and is seen as an invader by the body's immune system, resulting in the rejection of the tissue bearing those cells. This is particularly important in the case of transplanted tissue, because it could lead to transplant rejection. Because of the importance of HLA in transplantation, the HLA loci are some of the most frequently typed by serology and PCR.

Leukocyte and Lymphocyte.

HLA types are inherited, and some of them are connected with autoimmune disorders and other diseases.

Leukocyte and Lymphocyte.

Scientists at the Stanford University School of Medicine found that "Ionizing radiation can functionally alter the immune system and break self-tolerance"(a technical term for when radiation breaks down the normal ability to fight off disease). The study is published in the Journal of Immunology. The researchers irradiated the thymus and the peripheral lymphoid organs/tissues in mice to induce the autoimmune response. Total lymphoid irradiation on mice caused various organ-specific autoimmune diseases, such as gastritis, thyroiditis, and orchitis, depending on the radiation dosages, the extent of lymphoid irradiation, and the genetic background of the mouse strains. They concluded, "these results indicate that high dose, fractionated ionizing radiation on the lymphoid organs/tissues can cause autoimmune disease by affecting the T cell immune system."

Leukocyte and Lymphocyte.

A lymphocyte is one of the subtypes of white blood cell in a vertebrate's immune system. They include natural killer cells (NK cells) (which function in cell-mediated, cytotoxic innate immunity), T cells (for cell-mediated, cytotoxic adaptive immunity), and B cells (for humoral, antibody-driven adaptive immunity).

Leukocyte and Lymphocyte.

Cell mediated immunity is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Historically, the immune system was separated into two branches: humoral immunity, for which the protective function of immunization could be found in the humor (cell-free bodily fluid or serum) and cellular immunity, for which the protective function of immunization was associated with cells. CD4 cells or helper T cells provide protection against different pathogens. Cytotoxic T cells cause death by apoptosis without using cytokines, therefore in cell-mediated immunity cytokines are not always present.

Leukocyte and Lymphocyte.

Cellular immunity protects the body by: activating antigen-specific cytotoxic T-lymphocytes that are able

to induce apoptosis/ necrosis in body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, autoimmune cells, irradiated cells, isolated from irradiated mammals, and cancer cells displaying tumor antigens;

activating macrophages and natural killer cells, enabling them to destroy pathogens; and

stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses.

Leukocyte and Lymphocyte.

A cytotoxic T cell (also known as TC, cytotoxic T lymphocyte, CTL, T-killer cell, cytolytic T cell, CD8+ T-cells or killer T cell) is a T lymphocyte (a type of white blood cell) that kills cancer cells, cells that are infected (particularly with viruses), or cells that are damaged in other ways for example by radiation.

Most cytotoxic T cells express T-cell receptors (TCRs) that can recognize a specific antigen. An antigen is a molecule capable of stimulating an immune response, and is often produced by cancer cells or viruses. Antigens inside a cell are bound to class I MHC molecules, and brought to the surface of the cell by the class I MHC molecule, where they can be recognized by the T cell. If the TCR is specific for that antigen, it binds to the complex of the class I MHC molecule and the antigen, and the T cell destroys the cell.

In order for the TCR to bind to the class I MHC molecule, the former must be accompanied by a glycoprotein called CD8, which binds to the constant portion of the class I MHC molecule. Therefore, these T cells are called CD8+ T cells.

The affinity between CD8 and the MHC molecule keeps the TC cell and the target cell bound closely together during antigen-specific activation. CD8+ T cells are recognized as TC cells once they become activated and are generally classified as having a pre-defined cytotoxic role within the immune system. However, CD8+ T cells also have the ability to make some cytokines.

Leukocyte and Lymphocyte.

With an exception of some cell types, such as non-nucleated cells (including erythrocytes), Class I MHC is expressed by all host cells. When these cells are infected with a virus(or another intracellular pathogen), the cells degrade foreign proteins via antigen processing. These result in peptide fragments, some of which are presented by MHC Class I to the T cell antigen receptor (TCR) on CD8+ T cells.

The activation of cytotoxic T cells is dependent on several simultaneous interactions between molecules expressed on the surface of the T cell and molecules on the surface of the antigen-presenting cell (APC). For instance, consider the two signal model for TC cell activation.

Leukocyte and Lymphocyte.

First Signal – TCR - peptide-bound MHC class I molecule - There is a second interaction between the CD8 co-receptor and the class I MHC molecule to stabilize this signal.

Second Signal - CD28 molecule on the T cell - either CD80 or CD86 (also called B7-1 and B7-2) - CD80 and CD86 are known as costimulators for T cell activation. This second signal can be assisted (or replaced) by stimulating the TC cell with cytokines released from helper T cells.

Leukocyte and Lymphocyte.

A simple activation of naive CD8+ T cells requires the interaction with professional antigen-presenting cells, mainly with matured dendritic cells. To generate longlasting memory T cells and to allow repetitive stimulation of cytotoxic T cells, dendritic cells have to interact with both, activated CD4+ helper T cells and CD8+ T cells.[1][2] During this process, the CD4+ helper T cells "license" the dendritic cells to give a potent activating signal to the naive CD8+ T cells.

Leukocyte and Lymphocyte.

While in most cases activation is dependent on TCR recognition of antigen, alternative pathways for activation have been described. For example, cytotoxic T cells have been shown to become activated when targeted by other CD8 T cells leading to tolerization of the latter.

Once activated, the TC cell undergoes clonal expansion with the help of the cytokine Interleukin-2 (IL-2), which is a growth and differentiation factor for T cells. This increases the number of cells specific for the target antigen that can then travel throughout the body in search of antigen-positive somatic cells.

Leukocyte and Lymphocyte.

When exposed to infected/dysfunctional somatic cells, TC cells release the cytotoxins perforin, granzymes, and granulysin.

Through the action of perforin, granzymes enter the cytoplasm of the target cell and their serine protease function triggers the caspase cascade, which is a series of cysteine proteases that eventually lead to apoptosis(programmed cell death).

Leukocyte and Lymphocyte.

A second way to induce apoptosis is via cell-surface interaction between the TC and the infected cell. When a TC is activated it starts to express the surface protein FAS ligand(FasL)(Apo1L)(CD95L), which can bind to Fas (Apo1)(CD95) molecules expressed on the target cell. However, this Fas-Fas ligand interaction is thought to be more important to the disposal of unwanted T lymphocytes during their development or to the lytic activity of certain TH cells than it is to the cytolytic activity of TC effector cells. Engagement of Fas with FasL allows for recruitment of the death-induced signaling complex (DISC). The Fas-associated death domain (FADD) translocates with the DISC, allowing recruitment of procaspases 8 and 10. These caspases then activate the effector caspases 3, 6, and 7, leading to cleavage of death substrates such as lamin A, lamin B1, lamin B2, PARP (poly ADP ribose polymerase), and DNAPK (DNA-activated protein kinase). The final result is apoptosis of the cell that expressed Fas.

Leukocyte and Lymphocyte.

One of the functions of the immune system is to recognize and destroy abnormal or infected cells to maintain homeostasis. This is accomplished by cytotoxic lymphocytes. Cytotoxicity is a highly organized multifactor process. Here, we reviewed the apoptosis pathways induced by the two main cytotoxic lymphocyte subsets, natural killer (NK) cells and CD8+ T cells. In base to recent experimental evidence, we reviewed NK receptors involved in recognition of target-cell, as well as lytic molecules such as perforin, granzymes-A and -B, and granulysin.

Cell Mol Immunol. 2009 Feb;6(1):15-25. doi: 10.1038/cmi.2009.3. Cell death mechanisms induced by cytotoxic lymphocytes. Chávez-Galán L1, Arenas-Del Angel MC, Zenteno E, Chávez R, 

Lascurain R.

Leukocyte and Lymphocyte.

Granulysin is a human cytolytic molecule present in cytotoxic granules with perforin and granzymes. Recombinant 9-kDa granulysin kills a variety of microbes, including bacteria, yeast, fungi, and parasites, and induces apoptosis in tumor cells by causing intracellular calcium overload, mitochondrial damage, and activation of downstream caspases.

J Immunol. 2011 Mar 15;186(6):3497-504. doi: 10.4049/jimmunol.1003409. Epub 2011 Feb 4.

Granulysin delivered by cytotoxic cells damages endoplasmic reticulum and activates caspase-7 in target cells.

Saini RV1, Wilson C, Finn MW, Wang T, Krensky AM, Clayberger C.

Leukocyte and Lymphocyte.

Cytotoxic T lymphocytes (CTLs) provide potent defences against virus infection and intracellular pathogens. However, CTLs have a dark side — their lytic machinery can be directed against selftissues in autoimmune disorders, transplanted cells during graft rejection and host tissues to cause graft-versus-host disease, which is one of the most serious diseases related to CTL function. Although this duplicitous behaviour might seem contradictory, both beneficial and detrimental effects are the result of the same effector proteins. So, an understanding of the mechanisms that are used by CTLs to destroy targets and a knowledge of pathogen immuneevasion strategies will provide vital information for the design of new therapies. CYTOTOXIC T LYMPHOCYTES: ALL ROADS LEAD TO DEATH Michele Barry* and R. Chris Bleackley‡

Leukocyte and Lymphocyte.

Cytotoxic T lymphocytes mediate lysis of target cells by various mechanisms, including exocytosis of lytic proteins (perforin, granzymes) and receptor-ligand binding of Fas/APO molecules. Death of target cells is characterized by either necrosis or apoptosis, depending on the killing mechanism used and on the metabolism of the target cell itself.

Killing Mechanisms of Cytotoxic T Lymphocytes Peter Groscurth, Luis Filgueira Physiology Published 1 February 1998 Vol. 13 no. 1, 17-21 DOI:

Leukocyte and Lymphocyte.

The lysis of target cells via CTL proceeds through a sequence of programmed steps, including killer-target cell binding, delivery of the lethal hit, target cell lysis, and killer cell recycling. After recognition of the appropriate antigen, the CTL bind firmly to the surface of the target cell, an event that depends on the presence of Mg2+ but not Ca2+. The subsequent lysis of the target cells is mediated by two different mechanisms: exocytosis of lytic proteins and/or receptor-ligand binding of Fas/APO molecules.

The various pathways may result in different types of target cell death: necrosis and apoptosis.

http://physiologyonline.physiology.org/content/13/1/17

Leukocyte and Lymphocyte.

Lysosomes of CTL have a unique morphology that can be seen only by electron microscopy . Each granule has an electron-dense core surrounded by small, round vesicles. Within the core, several types of lytic proteins are stored in an inactive form. Upon binding of the effector cell to the target cell, the lysosomes are directed toward the contact area by reorientation of the microtubule organization center. Subsequently, the content of the granules is released into the intercellular space via exocytosis. Cytolysis of target cell is then mediated by two types of lytic proteins, perforin and granzymes, that act either alone or in combination with each other.

http://physiologyonline.physiology.org/content/13/1/17

Leukocyte and Lymphocyte.

In cancer patients undergoing radiation therapy, the beneficial effects of radiation can extend beyond direct cytotoxicity to tumor cells. Delivery of localized radiation to tumors often leads to systemic responses at distant sites, a phenomenon known as the abscopal effect which has been attributed to the induction and enhancement of the endogenous anti-tumor innate and adaptive immune response. The mechanisms surrounding the abscopal effect are diverse and include trafficking of lymphocytes into the tumor microenvironment, enhanced tumor recognition and killing via up-regulation of tumor antigens and antigen presenting machinery and, induction of positive immunomodulatory pathways. Here, we discuss potential mechanisms of radiation-induced enhancement of the anti-tumor response through its effect on the host immune system and explore potential combinational immune-based strategies such as adoptive cellular therapy using ex vivo expanded NK and T cells as a means of delivering a potent effector population in the context of radiation-enhanced anti-tumor immune environment.

The Effect of Radiation on the Immune Response to Cancers Bonggoo Park 1 , Cassian Yee 2 and Kyung-Mi Lee 1,*

Leukocyte and Lymphocyte.

http://www.intechopen.com/books/current-topics-in-ionizing-radiation-research/radiation-toxins-molecular-mechanisms-of-toxicity-and-radiomimetic-properties-

Acute Radiation Disease (ARD) or Acute Radiation Syndromes (ARS) are defined as the collective toxic clinical states observed from the acute pathological processes in various doses of irradiated mammals; to include: systemic inflammatory response syndrome (SIRS), toxic multiple organ injury (TMOI), toxic multiple organ dysfunction syndromes (TMODS), and finally, toxic multiple organ failure (TMOF). Moderate and high doses of radiation induces necrosis of radiosensitive cells with the subsequent formation of radiation toxins and their induced acute inflammatory processes. Radiation necrosis is the most substantial and most severe form of radiation induced injury, and when widespread, has grave therapeutic implications . Low doses of radiation exposure induces apoptosis (controlled, programmed death of radiosensitive cells) without significant levels of specific radiation-induced toxin formation and with only low levels of inflammatory response