User:CarstynJoiner/Effector cells

Effector Cells of the Immune System
Effector cells of the immune system are the various cells of the innate immune response and the adaptive immune response that respond to stimulus and bring about change to add to the body's effort to eliminate pathogens.

Examples of effector cells include:


 * Macrophage- effector cell of the innate immune response
 * Polymorphonuclear Leukocytes (PMNs), also referred to as granulocytes- effector cells of the innate immune response
 * Natural Killer Cells- effector cell of the innate immune response
 * Effector T Cells- effector cells of the adaptive immune response

Macrophage
A macrophage is a large phagocytic cell of the innate immune system. Derived from monocytes, macrophages are white blood cells located in tissue. They are found throughout the body in almost all tissues and organs, but they are rarely found in the bloodstream. Macrophages play an essential role in the immune system. Macrophages aid in preventing infection and injury; they do this using phagocytosis. This means that they engulf and degrade anything foreign to the body including but not limited to dead cells, debris, tumor cells and other foreign materials. Macrophages also play an important role in maintaining homeostasis by disposing internal waste materials and aiding in tissue repair.

There are two types of macrophages: M1 macrophages and M2 macrophages. M1 macrophages, also referred to as classically activated macrophages, promote inflammation. M1 macrophages secrete pro-inflammatory cytokines and chemokines, and present antigens. This is what allows them to act as an immune monitor. M1 macrophages promote a positive immune response. Conversely, M2 macrophages, commonly referred to as alternatively activated macrophage, reduce inflammation. M2 macrophages secrete anti-inflammatory cytokines including Arginase-I, IL-10, and TGF-β. This allows them to reduce inflammation and contribute to tumor growth. Overall, M2 macrophages play a crucial role in wound healing and tissue repair.

Polymorphonuclear Leukocytes (PMNs)
Polymorphonuclear Leukocytes (PMNs), also referred to as granulocytes, are immune cells that have granules that release enzymes during an immune response, allergic reaction, and asthma attacks. PMNs are a type of white blood cell. PMNs include neutrophils, basophils, and eosinophils.

Neutrophils
Neutrophils are the most abundant leukocyte in serum. They provide defense against infection and are the first responder against infection. After receiving the appropriate signals, neutrophils leave the bloodstream to go to the site of infection. There, they engulf dead cells or cells that are foreign to the body. Neutrophils can also degranulate to release chemicals, such as perforin, or proteases to damage pathogens. Neutrophils die after phagocytosis and will then be cleaned up by macrophages.

Basophils
Basophils are the least common type of PMN, but they are the largest type of granulocyte. Although they are produced in the blood marrow, basophils also circulate in the bloodstream. Activated when the antigen‐specific IgE antibodies recognize allergens bind to the basophils' high‐affinity IgE receptors, basophils help trigger acute and chronic allergic reactions by releasing histamine. Because of this, basophils play a significant role in anaphylaxis and medical conditions like asthma. Basophils are increased in response to these inflammatory responses. Sharing common features with mast cells, basophils and mast cell perform similar roles in allergic reactions and the immune response against parasites.

Eosinophils
Eosinophils are a type of white blood cell. They are granulocytes which means that they release granules of enzymes to defend the body against infection or foreign substances. Eosinophils are responsible for regulating immune responses in a variety of target tissues due to their large variety of cytokine and granule products. Eosinophils have two important functions: killing parasites, bacteria, or viruses that invade the body and promoting inflammation. Alongside mast cells and basophils, eosinophils are a mediator of allergic responses and asthma.

Natural Killer Cells (NK Cells)
Natural killer cells (NK cells) are lymphocytes in the innate immune system. These cells mature in the bone marrow and are released into the bloodstream. They are known as “natural killers” because it was thought that they did not need cytokine activation, but that has since been proven to be untrue. NK cells rapidly respond to virus-infected cells or abnormal cell growth with a cytotoxic response. All normal cells produce Major Histocompatability Complex I (MHC 1) which tells the immune system that they are a normal part of the organism’s body. NK cells target cells that have few to no MHC 1. MHC 1 inhibits the NK cells ability to begin its killing response by binding to its inhibitory receptor. When there is no MHC 1 on the cell surface or the MHC 1 that is not native to the organism, the killing response is activated. NK cells are cytotoxic which means that there are granzymes, small granules in their cytoplasm, that will signal apoptosis or cell lysis in abnormal cells.

CD8 Cytotoxic T cells
When CD8 Cytotoxic T cells are stimulated to differentiate they become the foot soldiers of the adaptive immune response The CTLs leave the lymph node where they are activated and migrate to the infection site. The Cytotoxic T-cells (CTLs) are tightly controlled by three different safeguards. This includes MHC class restriction, antigen recognition and self recognition. These are vital because the CTLs form an immunological synapse that secretes cytolytic molecules such as perforin and granzymes to induce apoptosis. The cytotoxic T-cells have the ability to target any nucleated self-cell that is virally infected.

CD4 T H 1 cells
When CD4 molecules have received both activation signals, the first signal from the T-cell receptor complex and MHC Class II receptor and the second signal from the CD28 receptor binding to the B7 ligand, and there is IFN-γ present, T H 1 differentiation occurs. The T H 1 leaves the lymph node and travels to the infection site where it can meet macrophages. If the adaptive immune response is being triggered, that means the macrophage (an effector cell of innate response) has been overwhelmed. T H 1 engage with macrophages to enhance their overall performance. They induce these changes in the macrophage by secreting cytokines via an immunological synapse. These secreted cytokines send messages to the macrophage to allow the phagolysosomes, containing the captured pathogen, to more easily fuse with lysosomes to increase their degradation and elimination from the body. A second effect is the increase in synthesis of important antimicrobials such as oxygen radicals nitric oxide and proteases to destroy pathogen. The T H 1 cell mediates effects by means of secreting cytokines to enhance the performance of basophils and eosinophils to eliminate the parasitic infection.

CD4 T H 2 cells
When CD4 molecules have received both activation signals, the first signal from the T-cell receptor complex and MHC Class II receptor and the second signal from the CD28 receptor binding to the B7 ligand, and there is IL-4 present, T H 2 differentiation occurs. T H 2 leaves the lymph node and travels to the infection site. At the infection site, T H 2 can meet with basophils, eosinophils and B cells to help the response to parasitic infection. They form an immunological synapse and the cytokines can be secreted to enhance the performance of basophils and eosinophils. There is also new research that points to their possible involvement in allergy asthma

CD4 T H 17 cells
When CD4 molecules have received both activation signals, the first signal from the T-cell receptor complex and MHC Class II receptor and the second signal from the CD28 receptor binding to the B7 ligand, and there is IL-17 present, T H 17 differentiation occurs. T H 17 leaves the lymph node and migrates to the infection site. At the infection sire they are able to enhance the neutrophil response to extracellular and fungal infection. T H 17 have only recently been identified as distinct from T H 1 and  T H 2 cells, this could be a result of some pathogens developing T H 1 and T H 2 immunity requiring the need for a different type of CD4 T-cell to help eliminate the pathogen.

CD4 T FH cells
When CD4 molecules have received both activation signals, the first signal from the T-cell receptor complex and MHC Class II receptor and the second signal from the CD28 receptor binding to the B7 ligand, and there is IL-21 present, T FH differentiation occurs. T FH cells remain in the lymph node, but they do migrate to the B-cell area of the lymph node. Here they can mitigate their effects. They engage with B-cells to help activate them to create antibodies. There are two distinct benefits of this interaction. The first effect is the T FH helps the process of somatic hypermutation, which results in higher affinity antibodies. He second is it aides the process of class switching. This results in antibodies that are better equipped to deal with different pathogens. In summary T FH cells help increase antibody efficiency and performance by simulating the B-cells.

CD4 T reg cells
When CD4 molecules have received both activation signals, the first signal from the T-cell receptor complex and MHC Class II receptor and the second signal from the CD28 receptor binding to the B7 ligand, and there is IL-21 present, Treg differentiation occurs. Treg cells have a distinct function from the other subtypes of T-cells. The target of Treg cells is to dampen the effects of the other immune system effector cells. They are believed to have distinct interactions that allow them to exert their functions. The first is in the lymph node that is generating the response. Here, they interact with dendritic cells to prevent them from interacting with other naïve T cells to prevent any further T-cell activation. The second is by interacting directly with other effector T cells to prevent them from secreting their cytotoxins(CD8 T cells) and cytokines (CD4 T cells). They are ultimately immunosuppressive.