User:Lmmcarle55/sandbox

(Section for Dendrobatidae page)

Other functional trade-offs are seen in poison frog toxin defense mechanisms relating to toxin resistance. Target-site insensitivity to the potent toxin epibatidine on nicotinic acetylcholine receptors provides a toxin resistance while reducing the affinity of acetylcholine binding.

(section for the phantasmal poison frog page)

Phantasmal poison frogs live in a similar areas to Epipedobates machalilla yet the two to occupy different environmental niches, and their population distribution is small and overlaps with that of E. machalilla. Genetic analysis places E. tricolor clades within E. machalilla and suggests that the phantasmal poison frog diverged recently via either peripheral speciation or high phenotypic divergence.

(section for E. Machalilla)

Epipedobates Machalilla displays a cryptic phenotype despite being in the otherwise aposematic family Epipedobates and likely lost an aposematic trait that evolved when Epipedobates first diverged. However, it is believed that with the high intra-specific phenotypic diversity observed within poison frogs and the role of diet in toxicity that there could be chemically defended E. machalilla populations.

// November 10, 2018 - Evolution Poison Frog Wikipedia Contribution

Article Evaluation

The article is very brief and lacking some information but the previous author clearly stated the basic role of lymphocyte homing receptors.

Two sources are cited and linked yet only one of them is accessible

"Stub" rating

There are several wikipedia pages linked to the lymphocyte homing receptor article offering thorough descriptions of cell adhesion molecules,

addressins, T and B lymphocytes etc.

>these are important to read before understanding the lymphocyte homing receptor reading

Bibliography

a little old but a very broad overview of lymphocyte homing receptors and their control on monocyte migration.

Discusses "sulfated glycans control of lymphocyte homing"

lymphocyte trafficking and homing in context of autoimmune diseases

Describes main proteins and integrins involved in lymphocyte homing & difference between naive and mature lymphocyte homing

Article discusses the structure and behaviors of a4B7 integrin to mediate lymphocyte rolling adhesion

The main text

Talks about HEV and lymphocyte homing (review)

Current Article (italics)

Lymphocyte homing refers to adhesion of the circulating lymphocytes in blood to specialized endothelial cells within lymphoid organs. Lymphocyte homing receptors are cell adhesion molecule glycoproteins of roughly 90kd in length expressed on lymphocyte cell membranes which recognize addressins on target tissues. These diverse tissue-specific adhesion molecules on lymphocytes contribute to the development of unique immune responses in humans.

Free lymphocytes constantly recirculate in blood after their re-entry from lymphoid tissue, via lymphatic and thoracic ducts. This happens s o that the full repertoire of antigenic specificities of lymphocytes is continuously represented throughout the body. Homing happens in tissue-specific manner—e.g. B lymphocytes migrate better to mucosa-associated lymphoid tissue (Peyer's patches), and T lymphocytes preferentially to the peripheral lymph nodes.[2]

The process of lymphocyte homing is deliberate, mediated by lymphocyte-endothelial recognition mechanisms that enable antigen-specific immune responses. Lymphocyte homing receptor control of organ-specific lymphocyte trafficking is considered to prevent autoreactivity in immune responses during B and T cell differentiation. Recently, lymphocyte homing has become a topic of interest for investigation of treatments for multiple sclerosis, type 1 diabetes mellitus, leukemia, and psoriasis.[3][5]

Naive lymphocyte Homing

Naive lymphocytes are able to circulate into secondary lymphoid tissues, Peyer’s patches, lymph nodes, and the spleen. Because they have not yet been exposed to antigen, these lymphocytes are undifferentiated and express few homing receptors.

High endothelial venules (HEVs) are cells found in secondary lymphoid organs that express large quantities of cell adhesion molecules, enabling undifferentiated lymphocytes to bind.[3] After entering lymph nodes and Peyer’s patches via HEVs, naive T and B cells are exposed to antigen circulating in lymph and differentiate to then contribute to adaptive immune response. HEVs develop from cytokine production after exposure to antigen and express adhesion molecules from the selectin family, mucin-like family, and the Ig super family.[8] Naive lymphocyte extravasation into Peyer’s patches is often mediated by L-selectin and their limited expression of alpha integrins and other homing receptors prevents them from accessing mucosal effector tissue.[6]

Mature lymphocyte homing

Mature lymphocytes are constantly recirculating in the blood and can traffic to secondary lymphoid tissue as well as target tissue including mucosal tissues of the lamina propria, inflammation, and other “extralymphoid immune effector sites”[6]. Lymphocyte homing receptor expression is altered by antigen exposure. This function enables the adaptive immune system to specialize an immune response in different parts of the body.

Upon exposure to antigens, lymphocytes lack homing ability during a period of sessile differentiation and cell division and antigen specific lymphocytes are stored in the spleen for 1-3 days. Subsequently, antigen-stimulated B and T cells express homing receptors particularly for the HEV in initial site of immunization tissue.[3]Furthermore, lymphocytes can alter cell adhesion molecule “activatability” to increase binding ability.[6] Organ-specific lymphocyte homing is important for antigen-specificity and in avoiding autoimmune “cross-reactions”[3].

Lymphocyte Homing and extravasation mechanism:

Lymphocyte homing occurs in four steps leading to extravasation into target tissue; Rolling, activation, activation-dependent “arrest”, and diapedesis [6]. Mediated by lymphocyte receptors and vascular ligand interactions, “tethering” is a reversible linkage that leads to either rolling along the vessel wall or transient immediate arrest. L-selectin is able to mediate vessel adhesion whereas a4 integrins, a4B1 or a4B7, can perform primary or secondary adhesion through a stronger tethering and even contribute to transendothelial migration of lymphocytes. L-selectin for example is also able to be cleaved by an enzyme, ensuring proper binding of lymphocytes and allowing release of non-target cells. While attached to the vessel, lymphocytes test target tissue for chemokines and pro-adhesive factors that then prompt “arrest.” In addition to a4 integrins, LFA-1 and MAC-1 mediate stopping of lymphocytes before transendothelial migration into target tissues. While initial adhesion indicates the start of lymphocyte homing, there is regulation of each step of extravasation.

Examples of Lymphocyte Homing Receptors:

a4b7 is an a4 integrin class homing receptor that targets lymphocytes in the gut expressing mucosal adhesion molecule-1(MAdCAM-1), mostly expressed in Peyer’s patches. [7] Additionally, a4B1 with the ligand vascular adhesion molecule-1(VCAM-1) function in lymphocyte trafficking and inflammation. [7]

Two other well known Lymphocyte Homing Receptors are CD34 and GLYCAM-1.