skin problems and diseases

Immunology in the skin.

The skin is the body’s main barrier against physical insults and microbial pathogens. Diverse and functionally specialized subsets of immune cells in the skin sense and respond to infection or various barrier breaches to activate an immune response and eventually, return to homeostasis. However, deregulated immune responses can also cause skin disorders, such as psoriasis.

Skin is the main barrier of the bodyagainst physical abuse and microbial
pathogens, it is a uniqueenvironment in which immune cells
interact with skin cells to maintaintissue homeostasis and induction of immune.

The answers that make up the skiepidermis of the dermis and subcutaneous. Fat area commensal bacteria, fungi and viruses living on the skin beneficial effect on protection against pathogens and for wound healing the epidermis is very specialized epithelial cells known as
keratinocytes they are continuously.


From just one layer of the basalke ratinocytes that often divide
dead cells, called patches of the cornea, form outer layer and mainly
responsible for the barrier function skin in the cells of the dermis, known as fibroblasts secrete elastin and collagen.

Fibers that form a dense extracellular matrix blood capillaries irrigate
dermis during lymph drainage through the lymphatic vessels to the lymph node specialized immune structures, in which immune cells are activated after the pathogen meets a diverse and functionally specialized immune cells colonize the skin in the epidermis.


Specialized subset of dendritic cells so-called Langerhans cell antigen sample, they project dendrites up to qualified epithelial layer and
samples of bacterial antigens such as toxins Langerhans cells seem
anti-inflammatory and activator ii depending on the dendritic cells of the dermis.


Effective in capturing dead cells and presenting antigen, such as viruses, others intracellular pathogens or skin associated autoantigen with T cells
dendritic cells are immune Guardians T cells are healthy immune effectors.


The skin contains more than twice, as much T-lymphocytes in the blood are the most these are memory T cells that have a previously encountered antigen and may Rapidly reactivate T cells in the epidermis is mainly composed of cd8 T lymphocytes.


Subset that becomes cytotoxic and kills target cells when activated
long-term stay in the epidermis, mostly disconnected from circulation
T cells in the dermis are mainly helpers cd4 T cells that have more
role in the immune response of various other immune cells, such as natural
killer cells.


Eosinophils and mast cells are present in the dermis and may be involved in allergic reactions in dendritic cutaneous cells and keratinocytes sense tissue, injuries such as wounds or cold sores lesions arising from latent herpes.


The virus reactivates and they do it through evolutionarily preserved
pathogen recognition receptors derived molecular structures or host
derivatives of the molecule that are exposed cell death, such as keratinocytes DNA.


Produce antimicrobial peptides that can kill bacteria that cause inflammation mediators such as interleukin 1 or IL-1, which activate dendritic cells and chemokines that attract neutrophils macrophages and T cells are activated.


Dendritic cells migrate to the lymph nodes where they present antigen from site of infection of naive T cells forcing them to activate and
differentiate into effector T cells.
The activated T cells return to the skin and kill infected keratinocytes for control viral infection or emit signals, that attract additional immune effector cells.


After virus cleanup of cd8 memory T cells are stored in the epidermis to
provide immunity for future meetings with the same virus, immune responses can become impaired and cause skin appearance disorders, such as psoriasis or atopic dermatitis psoriasis is life-long inflammatory skin disease, characteristic:

  • scaly reddish plaque combination;
  • environmental and genetic factors;
  • increases susceptibility to disease;
  • physical injury or inflammation can cause acute injury;
  • antigenic trigger is unknown, but current models suggest highlighted;
  • keratinocytes can release their own DNA, which in combination with antimicrobial;
  • the peptide activates a site of dermal plasma or dendritic cells secrete a large amount;
  • antiviral mediator of interferon together with pro-inflammatory il-1
    alpha released by stress keratinocytes;
  • interferon activates dermal dendrites cells that promote T cell differentiation;
  • earliest recognizable change in affected skin – accumulation of T
    cells and dendritic cells around the blood;
  • vessels in the dermis clear:

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