1>neutrophils
2>monocytes
3>lymphocytes
4>basophils
Ans: ?Monocytes-More likely (yeah some confusion with Lymphocytes)
Plz read below--
Neutrophil: Critical function of neutrophils is the clearance of invading microbes and cellular debris in the wound area, although these cells also produce substances such as proteases and reactive oxygen species (ROS), which cause some additional bystander damage.
Macrophages: Play multiple roles in wound healing.
In the early wound, macrophages release cytokines that promote the inflammatory response by recruiting and activating additional leukocytes.
Macrophages are also responsible for inducing and clearing apoptotic cells (including neutrophils), thus paving the way for the resolution of inflammation.
As macrophages clear these apoptotic cells, they undergo a phenotypic transition to a reparative state that stimulates keratinocytes, fibroblasts, and angiogenesis to promote tissue regeneration (Meszaros et al., 2000; Mosser and Edwards, 2008).
In this way, macrophages promote the transition to the proliferative phase of healing.
T-lymphocytes: Migrate into wounds following the inflammatory cells and macrophages, and peak during the late-proliferative/early-remodeling phase.
The role of T-lymphocytes is not completely understood and is a current area of intensive investigation.
Several studies suggest that delayed T-cell infiltration along with decreased T-cell concentration in the wound site is associated with impaired wound healing, while others have reported that CD 4+ cells (T-helper cells) have a positive role in wound healing and CD8+ cells (T-suppressor-cytotoxic cells) play an inhibitory role in wound healing (Swift et al., 2001; Park and Barbul, 2004).
Interestingly, recent studies in mice deficient in both T- and B-cells have shown that scar formation is diminished in the absence of lymphocytes (Gawronska-Kozak et al., 2006). In addition, skin gamma-delta T-cells regulate many aspects of wound healing, including maintaining tissue integrity, defending against pathogens, and regulating inflammation. These cells are also called dendritic epidermal T-cells (DETC), due to their unique dendritic morphology. DETC are activated by stressed, damaged, or transformed keratinocytes and produce fibroblast growth factor 7 (FGF-7), keratinocyte growth factors, and insulin-like growth factor-1, to support keratinocyte proliferation and cell survival.
DETC also generate chemokines and cytokines that contribute to the initiation and regulation of the inflammatory response during wound healing. While cross-talk between skin gamma-delta T-cells and keratinocytes contributes to the maintenance of normal skin and wound healing, mice lacking or defective in skin gamma-delta T-cells show a delay in wound closure and a decrease in the proliferation of keratinocytes at the wound site (Jameson and Havran, 2007; Mills et al., 2008).
2>monocytes
3>lymphocytes
4>basophils
Ans: ?Monocytes-More likely (yeah some confusion with Lymphocytes)
Plz read below--
Neutrophil: Critical function of neutrophils is the clearance of invading microbes and cellular debris in the wound area, although these cells also produce substances such as proteases and reactive oxygen species (ROS), which cause some additional bystander damage.
Macrophages: Play multiple roles in wound healing.
In the early wound, macrophages release cytokines that promote the inflammatory response by recruiting and activating additional leukocytes.
Macrophages are also responsible for inducing and clearing apoptotic cells (including neutrophils), thus paving the way for the resolution of inflammation.
As macrophages clear these apoptotic cells, they undergo a phenotypic transition to a reparative state that stimulates keratinocytes, fibroblasts, and angiogenesis to promote tissue regeneration (Meszaros et al., 2000; Mosser and Edwards, 2008).
In this way, macrophages promote the transition to the proliferative phase of healing.
T-lymphocytes: Migrate into wounds following the inflammatory cells and macrophages, and peak during the late-proliferative/early-remodeling phase.
The role of T-lymphocytes is not completely understood and is a current area of intensive investigation.
Several studies suggest that delayed T-cell infiltration along with decreased T-cell concentration in the wound site is associated with impaired wound healing, while others have reported that CD 4+ cells (T-helper cells) have a positive role in wound healing and CD8+ cells (T-suppressor-cytotoxic cells) play an inhibitory role in wound healing (Swift et al., 2001; Park and Barbul, 2004).
Interestingly, recent studies in mice deficient in both T- and B-cells have shown that scar formation is diminished in the absence of lymphocytes (Gawronska-Kozak et al., 2006). In addition, skin gamma-delta T-cells regulate many aspects of wound healing, including maintaining tissue integrity, defending against pathogens, and regulating inflammation. These cells are also called dendritic epidermal T-cells (DETC), due to their unique dendritic morphology. DETC are activated by stressed, damaged, or transformed keratinocytes and produce fibroblast growth factor 7 (FGF-7), keratinocyte growth factors, and insulin-like growth factor-1, to support keratinocyte proliferation and cell survival.
DETC also generate chemokines and cytokines that contribute to the initiation and regulation of the inflammatory response during wound healing. While cross-talk between skin gamma-delta T-cells and keratinocytes contributes to the maintenance of normal skin and wound healing, mice lacking or defective in skin gamma-delta T-cells show a delay in wound closure and a decrease in the proliferation of keratinocytes at the wound site (Jameson and Havran, 2007; Mills et al., 2008).
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