Melanocyte adhesion mechanisms (update)

DJ,

    It's just a research conclusion.

    Shifting the contemporary research paradigm, new studies point to the fact that Non-segmental Vitiligo (NSV) is not caused by a dysfunctional immune system. It's true there is an interplay between the immune system and melanocytes, but only when they are roaming around after their detachment.

    Melanocytes have 2 adhesion mechanisms: (1) the main one: Integrin alpha5-beta1 and (2) the contingent one: CCN3→DDR1→Colagen-IV. The latter seems to be faulty in a genetically NSV predisposed person. The former is easily affected by physical traumas, oxidative stress, and stress hormones in any person, what is critical for NSV sufferers since they do not have the contingent mechanism working properly. The upper 2 pictures show both mechanisms working properly before and after the action of causative factors in normal skin. The lower 2 pictures show disruption in the main mechanism in vitiliginous skin, as well as the wrong behavior of the contingency mechanism after the action of the same causative factors.

    A genetically NSV predisposed person may live a whole life without triggering the disease. However, once Vitiligo is triggered it becomes hard to cure (not impossible) because melanocyte's main adhesion mechanism will constantly be threatened (1) by the action of friction and trauma in certain regions like knees, elbows, hands, feet, wrists, around the eyes, forehead and around the mouth, (2) facilitated by oxidative stress, and (3) accelerated by stress hormones.

    After NSV is triggered, the Koebner phenomenon or isomorphic response (mimetism theory) may explain the development pattern of new patches on the frictioned and traumatized areas, but otherwise normal skin, and these new patches are clinically identical to those in the diseased skin.

    It would be reasonable to think that new patches would regularly appear after NSV was triggered, because the human body learned how to detach (kill) melanocytes due to the "mimetism theory". Recent researches have also defined it as "killing memory effect".

    However, the truth is not exactly like this. The mimetism theory and/or the "killing memory effect" are directly connected to the presence of a protein called MIA. This protein is the exact organic compound that the human body learned to produce improperly in NSV predisposed people. Its presence in the skin is what detaches melanocytes. While the protein is there, the "killing memory effect" will remain.

    More details at: http://vitiligomap.com/vitiligo/vitiligo-causes

Replies

kevin July 12, 2016 at 12:45pm

Let's not forget genes respond to the environment they are bathed in!
DJ July 11, 2016 at 2:51pm

Not sure I understand what is going with that diagram. Could you ELI5 what the above diagram is trying to show?
- Robot > DJ July 11, 2016 at 5:59pm
  
  DJ,
  
      It's just a research conclusion.
  
      Shifting the contemporary research paradigm, new studies point to the fact that Non-segmental Vitiligo (NSV) is not caused by a dysfunctional immune system. It's true there is an interplay between the immune system and melanocytes, but only when they are roaming around after their detachment.
  
      Melanocytes have 2 adhesion mechanisms: (1) the main one: Integrin alpha5-beta1 and (2) the contingent one: CCN3→DDR1→Colagen-IV. The latter seems to be faulty in a genetically NSV predisposed person. The former is easily affected by physical traumas, oxidative stress, and stress hormones in any person, what is critical for NSV sufferers since they do not have the contingent mechanism working properly. The upper 2 pictures show both mechanisms working properly before and after the action of causative factors in normal skin. The lower 2 pictures show disruption in the main mechanism in vitiliginous skin, as well as the wrong behavior of the contingency mechanism after the action of the same causative factors.
  
      A genetically NSV predisposed person may live a whole life without triggering the disease. However, once Vitiligo is triggered it becomes hard to cure (not impossible) because melanocyte's main adhesion mechanism will constantly be threatened (1) by the action of friction and trauma in certain regions like knees, elbows, hands, feet, wrists, around the eyes, forehead and around the mouth, (2) facilitated by oxidative stress, and (3) accelerated by stress hormones.
  
      After NSV is triggered, the Koebner phenomenon or isomorphic response (mimetism theory) may explain the development pattern of new patches on the frictioned and traumatized areas, but otherwise normal skin, and these new patches are clinically identical to those in the diseased skin.
  
      It would be reasonable to think that new patches would regularly appear after NSV was triggered, because the human body learned how to detach (kill) melanocytes due to the "mimetism theory". Recent researches have also defined it as "killing memory effect".
  
      However, the truth is not exactly like this. The mimetism theory and/or the "killing memory effect" are directly connected to the presence of a protein called MIA. This protein is the exact organic compound that the human body learned to produce improperly in NSV predisposed people. Its presence in the skin is what detaches melanocytes. While the protein is there, the "killing memory effect" will remain.
  
      More details at: http://vitiligomap.com/vitiligo/vitiligo-causes

This reply was deleted.