Question: What are the cells of the immune system that are involved in protecting the body against both infectious disease and foreign invaders, where a disease of the eye in response to changes in the vitreous humor or more rarely, diabetes, that causes the cells response?

Context articles: Immunodeficiency
Adaptive immune system
Thymus
Antigenic variation
White blood cell
Memory T cell
Epiretinal membrane
Severe combined immunodeficiency
Gabrielle Belz
Artificial antigen presenting cells

Immunodeficiency (or immune deficiency) is a state in which the immune system's ability to fight infectious disease and cancer is compromised or entirely absent.
 Most cases of immunodeficiency are acquired ("secondary") due to extrinsic factors that affect the patient's immune system.
 Examples of these extrinsic factors include HIV infection, extremes of age, and environmental factors, such as nutrition.
 In the clinical setting, the immunosuppression by some drugs, such as steroids, can be either an adverse effect or the intended purpose of the treatment.
 Examples of such use is in organ transplant surgery as an anti-rejection measure and in patients suffering from an overactive immune system, as in autoimmune diseases.
 Some people are born with intrinsic defects in their immune system, or primary immunodeficiency.
 A person who has an immunodeficiency of any kind is said to be immunocompromised.
 An immunocompromised person may be particularly vulnerable to opportunistic infections, in addition to normal infections that could affect everyone.
 Immunodeficiency also decreases cancer immunosurveillance, in which the immune system scans the body's cells and kills neoplastic ones.
The adaptive immune system, also known as the acquired immune system or, more rarely, as the specific immune system, is a subsystem of the overall immune system that is composed of highly specialized, systemic cells and processes that eliminate pathogens or prevent their growth.
 The adaptive immune system is one of the two main immunity strategies found in vertebrates (the other being the innate immune system).
 Adaptive immunity creates immunological memory after an initial response to a specific pathogen, and leads to an enhanced response to subsequent encounters with that pathogen.
 This process of acquired immunity is the basis of vaccination.
 Like the innate system, the adaptive system includes both humoral immunity components and cell-mediated immunity components.
The thymus is a specialized primary lymphoid organ of the immune system.
 Within the thymus, T cells or T lymphocytes mature.
 T cells are critical to the adaptive immune system, where the body adapts specifically to foreign invaders.
 The thymus is composed of two identical lobes and is located anatomically in the anterior superior mediastinum, in front of the heart and behind the sternum.
 Histologically, each lobe of the thymus can be divided into a central medulla and a peripheral cortex which is surrounded by an outer capsule.
 The cortex and medulla play different roles in the development of T-cells.
 Cells in the thymus can be divided into thymic stromal cells and cells of hematopoietic origin (derived from bone marrow resident hematopoietic stem cells).
 Developing T-cells are referred to as thymocytes and are of hematopoietic origin.
 Stromal cells include epithelial cells of the thymic cortex and medulla, and dendritic cells.
Antigenic variation refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters its surface proteins in order to evade a host immune response.
 It is related to phase variation.
 Immune evasion is particularly important for organisms that target long-lived hosts, repeatedly infect a single host and are easily transmittable.
 Antigenic variation not only enables immune evasion by the pathogen, but also allows the microbes to cause re-infection, as their antigens are no longer recognized by the host's immune system.
 When an organism is exposed to a particular antigen (i.e. a protein on the surface of a bacterium) an immune response is stimulated and antibodies are generated to target that specific antigen.
 The immune system will then "remember" that particular antigen, and defenses aimed at that antigen become part of the immune system’s acquired immune response.
 If the same pathogen tries to re-infect the same host the antibodies will act rapidly to target the pathogen for destruction.
 However, if the pathogen can alter its surface antigens, it can evade the host's acquired immune system.
 This will allow the pathogen to re-infect the host while the immune system generates new antibodies to target the newly identified antigen.
 Antigenic variation can occur by altering a variety of surface molecules including proteins and carbohydrates.
 There are many molecular mechanisms behind antigenic variation, including gene conversion, site-specific DNA inversions, hypermutation, as well as recombination of sequence cassettes.
 In all cases, antigenic variation and phase variation result in a heterogenic phenotype of a clonal population.
 Individual cells either express the phase-variable protein(s) or express one of multiple antigenic forms of the protein.
 This form of regulation has been identified mainly, but not exclusively, for a wide variety of surface structures in pathogens and is implicated as a virulence strategy.
White blood cells (WBCs), also called leukocytes or leucocytes, are the cells of the immune system that are involved in protecting the body against both infectious disease and foreign invaders.
 All white blood cells are produced and derived from multipotent cells in the bone marrow known as hematopoietic stem cells. Leukocytes are found throughout the body, including the blood and lymphatic system.
Memory T cells are a subset of infection- as well as potentially cancer-fighting T cells (also known as a T lymphocyte) that have previously encountered and responded to their cognate antigen; thus, the term antigen-experienced T cell is often applied.
 Such T cells can recognize foreign invaders, such as bacteria or viruses, as well as cancer cells.
 Memory T cells have become "experienced" by having encountered antigen during a prior infection, encounter with cancer, or previous vaccination.
 At a second encounter with the invader, memory T cells can reproduce to mount a faster and stronger immune response than the first time the immune system responded to the invader.
 This behaviour is utilized in T lymphocyte proliferation assays, which can reveal exposure to specific antigens.
Epiretinal membrane is a disease of the eye in response to changes in the vitreous humor or more rarely, diabetes.
 It is also called macular pucker.
 Sometimes, as a result of immune system response to protect the retina, cells converge in the macular area as the vitreous ages and pulls away in posterior vitreous detachment (PVD).
 PVD can create minor damage to the retina, stimulating exudate, inflammation, and leucocyte response.
 These cells can form a transparent layer gradually and, like all scar tissue, tighten to create tension on the retina which may bulge and pucker (e.g., macular pucker), or even cause swelling or macular edema.
 Often this results in distortions of vision that are clearly visible as bowing ←→ when looking at lines on chart paper (or an Amsler grid) within the macular area, or central 1.0 degree of visual arc.
 Usually it occurs in one eye first, and may cause binocular diplopia or double vision if the image from one eye is too different from the image of the other eye.
 The distortions can make objects look different in size (usually larger = macropsia), especially in the central portion of the visual field, creating a localized or field dependent aniseikonia that cannot be fully corrected optically with glasses.
 Partial correction often improves the binocular vision considerably though.
 In the young (under 50 years of age), these cells occasionally pull free and disintegrate on their own; but in the majority of sufferers (over 60 years of age) the condition is permanent.
 The underlying photoreceptor cells, rod cells and cone cells, are usually not damaged unless the membrane becomes quite thick and hard; so usually there is no macular degeneration.
Severe combined immunodeficiency, SCID, also known as alymphocytosis, Glanzmann–Riniker syndrome, severe mixed immunodeficiency syndrome, and thymic alymphoplasia, is a rare genetic disorder characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations that result in heterogeneous clinical presentations.
 SCID involves defective antibody response due to either direct involvement with B lymphocytes or through improper B lymphocyte activation due to non-functional T-helper cells. Consequently, both "arms" (B cells and T cells) of the adaptive immune system are impaired due to a defect in one of several possible genes.
 SCID is the most severe form of primary immunodeficiencies, and there are now at least nine different known genes in which mutations lead to a form of SCID.
 It is also known as the bubble boy disease and bubble baby disease because its victims are extremely vulnerable to infectious diseases and some of them, such as David Vetter, have become famous for living in a sterile environment.
 SCID is the result of an immune system so highly compromised that it is considered almost absent.
Gabrielle Belz is an Australian molecular immunologist and viral immunologist.
 She is a faculty member of the Walter and Eliza Hall Institute of Medical Research, within the Molecular Immunology division.
 Belz has made important contributions to the understanding of immune system function, especially in relation to the molecular and cellular signalling pathways of immune response to viruses.
 Her research has focused on understanding the signals that drive the initial development of protective immunity against pathogen infections, such as influenza and herpes viruses.
 This includes research into how cytotoxic T cells (a type of T lymphocyte that destroys virally infected cells and tumor cells) recognise and remove virally-infected cells from the body following infection.
 Research into the description of the specific factors and response during infection will contribute towards the long term development of vaccines for infectious disease, and the development of better treatments for autoimmune diseases.
Artificial antigen presenting cells (aAPCs) are a new technology and approach to cancer immunotherapy.
 Immunotherapy aims to utilize the body’s own defense mechanism—the immune system—to recognize mutated cancer cells and to kill them the way the immune system would recognize and kill a virus.
 Antigen presenting cells are the sentinels of the immune system and patrol the body for pathogens.
 When they encounter foreign pathogens, the antigen presenting cells alert the T cells—“the soldiers of the immune system”—that there is something foreign in the body with specific cell surface molecules.
 aAPCs are synthetic versions of these sentinel cells and are made by attaching the specific T-cell stimulating signals to various macro and micro biocompatible surfaces.
 This can potentially reduce the cost while allowing control over generating large numbers of functional pathogen-specific T cells for therapy.
 Activated and stimulated T cells can be studied in this biomimetic contex and used for adoptive transfer as an immunotherapy.