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- The Semiotics of Cellular Communication in the Immune System
- IMMUNOLOGY A Short Course 7th Edition Pdf
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- The Semiotics of Cellular Communication in the Immune System
The Semiotics of Cellular Communication in the Immune System
The ability of the outer ocular system to recognize pathogens as foreign and eliminate them is critical to retain corneal transparency, hence preservation of sight.
Therefore, a combination of mechanical, anatomical, and immunological defense mechanisms has evolved to protect the outer eye. These host defense mechanisms are classified as either a native, nonspecific defense or a specifically acquired immunological defense requiring previous exposure to an antigen and the development of specific immunity.
Sight-threatening immunopathology with autologous cell damage also can take place after these reactions. This article discusses the innate and acquired corneal elements of the immune defense at the ocular surface. The relative roles of the various factors contributing to prevention of eye infection remain to be fully defined. The vertebrate cornea has a unique immune defense to protect against foreign material and a number of microbial pathogens.
As the epidermis and dermis protect underlying tissues of the body, the cornea must prevent injury to the delicate structures of the eye.
However beyond its protective function, the cornea has evolved to be a highly transparent tissue, which refracts light to enable high-resolution vision. In order for the cornea to maximally transmit light, the extracellular matrix of collagens and proteoglycans have become highly ordered, and all extraneous cells and blood vessels have been excluded.
The premium of enhancing visual acuity must have provided a selective advantage for early vertebrates.
Improved visual acuity would have increased the fitness of these animals and would have outweighed the disadvantage of having local immune cells and blood vessels at a distance where a time delay in addressing a central corneal infection could lead to blindness.
The first vertebrates were jawless fish that were believed to have evolved some million years ago. With better vision, these creatures were likely more active and predatory.
This advantage along with the later development of jaws enabled bony fish to flourish and establish other habitats. One such habitat was shallow waters where lunged fish made the transition to land several hundred thousand years later. The exposure of ocular surface to potentially harmful materials including microbes, and toxic substances found in the environment continually places the ocular surface at risk for immunologic events. There are two approaches to understanding immune defense at the corneal surface.
One is to study the cellular and molecular elements present in the human cornea for possible roles in mounting an immune defense. Peripheral dendritic cells or Langerhans cells, for example, have been studied for their global antigen presenting properties or keratocytes for their intrinsic microbial defensive peptides.
The other method is to investigate immune defensive pathways in a specific animal model of microbial infection. Well-known examples of this approach are studies performed with murine herpes simplex virus HSV and onchocerchiasis. Both approaches provide valuable information, but both have limitations.
For ethical reasons, studies of how the native human cornea responds to controlled experimental infections cannot be carried out. However, clinical descriptions and investigation of the progression of culture-proven corneal infections and the response to antimicrobials provide some concepts of how the immune system reacts.
For example, Neiserria gonorrhea keratitis can proceed rapidly to perforation suggesting that the local immune response is totally inadequate and is overwhelmed.
In contrast, helminthic keratitis proceeds slowly with infiltrates and with persistent recurrent disease leading to corneal neovascularization and scarring. In addition, corneas that have been excised for corneal transplantation or biopsy for a particular infection can be valuable for understanding what cells and signaling events are involved, using routine histopathology as well as more sophisticated methods such as immunohistochemistry, polymerase chain reaction, and immunoelectron microscopy.
Controlled infections in animal models may provide more detailed analysis of immune pathways, although murine or nonhuman primate experiments may not accurately reflect immune response to human disease.
Hence, information from both methods of study is valuable. Innate immunity is the first line of defense against corneal infection. Physical barriers, such as the bony orbit and the eyelids, guard against traumatic events, which could comprise the corneal surface.
Additionally, there are numerous cellular and molecular elements that constantly protect against inoculation of the corneal surface against microorganisms.
These elements include tears, corneal nerves, the epithelium, keratocytes, polymorphonuclear cells, and some cytokines. The main function of tears is to prevent drying of the cornea. In addition, tears flush foreign particles from the ocular surface, and transport antimicrobial proteins lactoferrin, lysozyme, lipocalin, and beta-lysin and immunoglobulins to the ocular surface to prevent infections.
Secretory IgA binds to bacteria and prevents bacterial adherence to epithelium. Tear IgG as well as IgA can neutralize some viruses and bind bacteria and hence play a role in corneal defense. Corneal epithelial cells actively and passively participate in protecting the ocular surface. These cells are capable of secreting cytokines to activate immune defenses to protect against microbial invasion. IL-1 R antagonist gene therapy, in experimental models, showed a decreased leucocyte infiltration, selectively altered the cytokine profile, and suppressed corneal neovascularization.
Keratocytes also have a defensive capacity during microbial invasion. Defensins hold therapeutic potential in ocular infections as they have a broad spectrum of antimicrobial activity against bacteria, fungi, and viruses and accelerate epithelial healing.
In HSV keratitis, IL-8 gene expression, a potent chemoattractant for neutrophils, by keratocytes has also been demonstrated. Corneal nerves are important in the innate defense of the cornea by relaying sensory information leading to reflexive movements to protect the eye.
Two neuropeptides, calcitonin gene-related peptide and substance P, are released from the termini of corneal sensory neurons in response to pain. Complement comprises a series of effector and regulatory proteins that activate each other in an orderly fashion to generate biologically active molecules, such as enzymes, opsonins, anaphylotoxins, and chemotaxins.
All seven complement components are more concentrated in the peripheral cornea as compared to the central cornea. This distribution may result from the diffusion of complement components from limbal vessels into the cornea. Interferons IFN are a group of proteins made by cells in response to viral infection, which induce a generalized antiviral state in the surrounding cells. INFs also stimulate production of major histocompatibility complex MHC class I molecules and proteins that enhance the ability of virally infected cells to present viral proteins to T cells.
Neutrophils are important in protecting the corneal epithelium from invasion by many microorganisms. Normally found in the cornea, neutrophils move through endothelial cells of the limbal vasculature by adhesion to receptors on vascular endothelial cells, a process called diapedesis. The neutrophil is a critical effector cell in innate immunity and plays vital roles in phagocytosis and microbial killing.
Eosinophils possess surface receptors for IgE and complement components. A number of eosinophil granule proteins, such as major basic protein and cationic protein, have been identified which are presumed to play a role in parasitic toxicity. Macrophages are important in the innate immune response against microbial infections as they have phagocytic and antigen presenting capabilities as well as secretion of inflammatory cytokines.
Although macrophages have traditionally been thought to reside in the conjunctiva, resident macrophages have been recently found in the murine corneal stroma and may play a part in host immune responses. NK cells are large granular lymphocytic cells and have no surface antigen receptors. As a consequence, NK cells lyse target cells that have lost or express insufficient amounts of MHC class I molecules, as frequently occurs in tumours, cells infected by certain viruses, antibody-coated cells, undifferentiated cells, and tumour cells.
In some cases, cell-mediated immunity can be out of proportion to the antigenic threat, leading to irreversible tissue destruction. Scarring and disorganization of the extracellular matrix as a result of HSV dermatitis may be inconsequential, whereas the same response in the cornea may lead to a significant permanent visual loss. Langerhans cells are essential sentinel cells that are part of the corneal immune surveillance system. After Langerhans cells recognize an antigen as nonself, the antigen is processed and is transported to the surface by MHC molecules, either class I or II.
Two subsets of T helper cells have been described with differential cytokine production profiles. Th1 cells are preferentially selected as participants in inflammatory reactions associated with delayed-type hypersensitivity reactions and low antibody production.
Th2 cells, on the other hand, are involved in inflammatory reactions associated with persistent antibody production, including allergic responses in which IgE production is predominant. Cytokines produced by Th cells are of critical importance for the outcome of many infectious diseases. For example in schistosomiasis, a Th1 response is associated with elimination of the parasite, whereas a Th2 response results in extensive disease and granuloma formation.
These events may be regulated by accumulation of particular cell populations at a site of immune response that can be regulated by the expression of specific chemokines. Immunologic differences exist between the peripheral and central cornea. The peripheral cornea being proximate to the conjunctiva has all of the immunologic machinery necessary to generate an immune response.
The peripheral cornea, possessing Langerhans' cells and IgM, also has more C1, the recognition unit of the classic pathway of complement, than the central cornea. Antigen—antibody complexes, whether formed in the cornea itself or whether derived from the tears, aqueous humour, or limbal vessels, may activate complement more effectively in the peripheral than central cornea. To follow are three examples of immune defense at the ocular surface to microbial invasion. Each organism provokes a different defensive response, but each has components of innate and acquired immunity that play a defensive role.
There are two defensive stages for each, an early and a late corresponding to innate and acquired immune responses, respectively. The first stage is an immediate response within minutes to several hours to microbial invasion. The innate immune system is charged with this initial defensive response, which always involves a neutrophilic infiltrate. If the initial defensive effort fails, adaptive immunity is called upon where Langerhans cells identify the foreign antigen in the cornea.
The full adaptive immune response, however, may take days. Many bacterial and fungal organisms have components of their cell membrane and walls that play a vital role in the maintaining viability and have been retained over millions of years. These conserved molecular signatures have been recognized by host immune systems as a sign of incipient microbial invasion and have evolved to elicit an immediate and intense neutrophilic hypersensitivity response.
Lipopolysaccharide LPS is another conserved molecule, a glycolipid in the outer membrane of Gram-negative bacteria including P. A toll-like receptor, TLR4, has been identified in corneal epithelial cells. Thus, the immune recognition of LPS as a conserved signature of Gram-negative bacterial invasion allows for the rapid influx of neutrophils from the perilimbal vessels.
Recruitment of neutrophils by MIP-2 in Pseudomonas -infected corneas has been demonstrated in susceptible mice.
Contact lens wear has been shown to be a risk factor for the development of Pseudomonas keratitis. An acquired immune defensive component may be a possible explanation for this risk factor as experimental contact lens wear can cause migration of Langerhans cells into the central cornea.
Herpes simplex keratitis HSK has many different clinical presentations. Replication of the virus in corneal epithelium produces a classic dendrite, while immune reactions to the virus in the stroma and endothelium can produce infiltration, ulceration, vascularization, or oedema. Peripheral ulcerative keratitis can also seen with the disease. The relation of the immune surface defenses and HSV is complex. There appears to be a balance of ameliorating and exacerbating immune factors to keep viral replication and release of proinflammatory cytokines in check without incurring sight-threatening corneal damage.
IMMUNOLOGY A Short Course 7th Edition Pdf
Functions of MHC in the Immune System. Download PDF Copy. Shelley Farrar Stoakes, daviesscountyarc.org, daviesscountyarc.org By Shelley Farrar Stoakes, daviesscountyarc.org, daviesscountyarc.org
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The Semiotics of Cellular Communication in the Immune System
A T cell is a type of lymphocyte. T cells are one of the important white blood cells of the immune system, and play a central role in the adaptive immune response. T cells can be easily distinguished from other lymphocytes by the presence of a T-cell receptor TCR on their cell surface. T cells are born from hematopoietic stem cells ,  found in the bone marrow. Then, developing T cells migrate to the thymus gland to mature.
Immunoglobulins, also called antibodies, are glycoprotein molecules that make up an important part of the immune system, which is responsible for fighting off infectious disease and foreign "invasions" more generally. Often abbreviated as "Ig," antibodies are found in blood and other bodily fluids of humans and other vertebrate animals. They help identify and destroy foreign substances such as microbes e. Only IgA, IgG and IgM are found in significant amounts in the human body, but all are important or potentially important contributors to the human immune response. Immunoglobulins are produced by B-lymphocytes, which are a class of leukocytes white blood cells. They are symmetrical Y-shaped molecules consisting of two longer heavy H chains and two shorter light L chains.
The HLA region encodes several molecules that play key roles in the immune system. The advances being made in determining the primary associations within the HLA region and AIDs will not only increase our understanding of the mechanisms behind disease pathogenesis but may also aid in the development of novel therapeutic targets in the future. These diseases are often chronic and debilitating and, although treatments are available, many are inadequate [ 1 ] providing the impetus for a greater understanding of the disease mechanisms and the development of novel therapeutic agents. Antigen presentation and T cell activation appear to be key to triggering an autoimmune response [ 2 ] prompting investigation of many genes within this pathway for association with AID including several within the major histocompatibility complex MHC.
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The fitness gains resulting from development of the adaptive immune system AIS during evolution are still the subject of hot debate. A large random repertoire of antigenic receptors is costly to develop and could be the source of autoimmune reactions.