Feb 2014 allergy a physiology

CME Co-ordinator à Abbotsford Regional Hospital
13 Jun 2014
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
Feb 2014 allergy a physiology
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Feb 2014 allergy a physiology

Notes de l'éditeur

  1. This disease affects nearly 1% of the population.
  2. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  3. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  4. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  5. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  6. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  7. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  8. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  9. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  10. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  11. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  12. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  13. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  14. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  15. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  16. a | Sensitization and memory. Initial contact with minute amounts of intact, soluble allergen at mucosal surfaces, particularly of the respiratory tract, might favour allergen uptake by potent antigen-presenting cells (for example, dendritic cells) and/or immunoglobulin-mediated capture by specific B cells. If T helper 2 (TH2)-cell help is acquired, cytokines such as interleukin-4 (IL-4) and IL-13 will be produced that favour immunoglobulin-class switching of specific B cells to immunoglobulin E (that is, sensitization). Sensitization leads to the establishment of IgE+ memory B cells and allergen-specific memory T cells. Subsequent repeated allergen contact will boost IgE+ memory B cells that receive T-cell help to produce increased levels of allergen-specific IgE antibodies. These are loaded by means of specific receptors (FcRI, high-affinity IgE receptor; FcRII, low-affinity IgE receptor) onto mast cells, basophils, monocytes, dendritic cells and B cells. b | Immediate reaction. The crosslinking of effector-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. c | Late reaction. This is caused by the presentation of allergens to T cells, which become activated, proliferate and release proinflammatory cytokines (for example, IL-4, IL-5 and IL-13). This process might be enhanced by the IgE-mediated presentation of allergens to T cells. TH2 cytokines (for example, IL-5) induce tissue eosinophilia and the release of inflammatory mediators from eosinophils. APC, antigen-presenting cell; DC, dendritic cell; TCR, T-cell receptor
  17. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  18. Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma.
  19. a | Sensitization and memory. Initial contact with minute amounts of intact, soluble allergen at mucosal surfaces, particularly of the respiratory tract, might favour allergen uptake by potent antigen-presenting cells (for example, dendritic cells) and/or immunoglobulin-mediated capture by specific B cells. If T helper 2 (TH2)-cell help is acquired, cytokines such as interleukin-4 (IL-4) and IL-13 will be produced that favour immunoglobulin-class switching of specific B cells to immunoglobulin E (that is, sensitization). Sensitization leads to the establishment of IgE+ memory B cells and allergen-specific memory T cells. Subsequent repeated allergen contact will boost IgE+ memory B cells that receive T-cell help to produce increased levels of allergen-specific IgE antibodies. These are loaded by means of specific receptors (FcRI, high-affinity IgE receptor; FcRII, low-affinity IgE receptor) onto mast cells, basophils, monocytes, dendritic cells and B cells. b | Immediate reaction. The crosslinking of effector-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. c | Late reaction. This is caused by the presentation of allergens to T cells, which become activated, proliferate and release proinflammatory cytokines (for example, IL-4, IL-5 and IL-13). This process might be enhanced by the IgE-mediated presentation of allergens to T cells. TH2 cytokines (for example, IL-5) induce tissue eosinophilia and the release of inflammatory mediators from eosinophils. APC, antigen-presenting cell; DC, dendritic cell; TCR, T-cell receptor
  20. a | Sensitization and memory. Initial contact with minute amounts of intact, soluble allergen at mucosal surfaces, particularly of the respiratory tract, might favour allergen uptake by potent antigen-presenting cells (for example, dendritic cells) and/or immunoglobulin-mediated capture by specific B cells. If T helper 2 (TH2)-cell help is acquired, cytokines such as interleukin-4 (IL-4) and IL-13 will be produced that favour immunoglobulin-class switching of specific B cells to immunoglobulin E (that is, sensitization). Sensitization leads to the establishment of IgE+ memory B cells and allergen-specific memory T cells. Subsequent repeated allergen contact will boost IgE+ memory B cells that receive T-cell help to produce increased levels of allergen-specific IgE antibodies. These are loaded by means of specific receptors (FcRI, high-affinity IgE receptor; FcRII, low-affinity IgE receptor) onto mast cells, basophils, monocytes, dendritic cells and B cells. b | Immediate reaction. The crosslinking of effector-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. c | Late reaction. This is caused by the presentation of allergens to T cells, which become activated, proliferate and release proinflammatory cytokines (for example, IL-4, IL-5 and IL-13). This process might be enhanced by the IgE-mediated presentation of allergens to T cells. TH2 cytokines (for example, IL-5) induce tissue eosinophilia and the release of inflammatory mediators from eosinophils. APC, antigen-presenting cell; DC, dendritic cell; TCR, T-cell receptor
  21. a | Sensitization and memory. Initial contact with minute amounts of intact, soluble allergen at mucosal surfaces, particularly of the respiratory tract, might favour allergen uptake by potent antigen-presenting cells (for example, dendritic cells) and/or immunoglobulin-mediated capture by specific B cells. If T helper 2 (TH2)-cell help is acquired, cytokines such as interleukin-4 (IL-4) and IL-13 will be produced that favour immunoglobulin-class switching of specific B cells to immunoglobulin E (that is, sensitization). Sensitization leads to the establishment of IgE+ memory B cells and allergen-specific memory T cells. Subsequent repeated allergen contact will boost IgE+ memory B cells that receive T-cell help to produce increased levels of allergen-specific IgE antibodies. These are loaded by means of specific receptors (FcRI, high-affinity IgE receptor; FcRII, low-affinity IgE receptor) onto mast cells, basophils, monocytes, dendritic cells and B cells. b | Immediate reaction. The crosslinking of effector-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. c | Late reaction. This is caused by the presentation of allergens to T cells, which become activated, proliferate and release proinflammatory cytokines (for example, IL-4, IL-5 and IL-13). This process might be enhanced by the IgE-mediated presentation of allergens to T cells. TH2 cytokines (for example, IL-5) induce tissue eosinophilia and the release of inflammatory mediators from eosinophils. APC, antigen-presenting cell; DC, dendritic cell; TCR, T-cell receptor
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