Immunological aspects of infections part 12



Immune System


Although it is clear that innate immunity is the first line of defense against invading organisms, the TLRs are also playing a role in adaptive immunity, and the dendritic cell (DC) appears to be playing a key role in linking the innate  and adaptive immune responses. As immature cells, they are present in the peripheral tissues. However, with the appearance of invading organisms, DCs recognize these pathogens through their TLRs. Fortunately, they express the full repertoire of TLRs. After activation of the TLRs, the DCs are transformed into more mature cells with high expression of major histocompatibility complex (MHC) and the co-stimulatory molecules CD80 and CD86. The DCs then migrate to the lymph nodes to activate antigen-specific naive T cells. The cytokine milieu being expressed around the cells determines their fate; that is, the production of IL-12 drives these cells to TH1 cells, which produce interferon δ, whereas  IL-4 drives them toward  TH2 cells producing IL-4, IL-5, IL-10 and IL-13. These latter cytokines are of interest as they are also responsible for the development of allergic diseases such as asthma  and account for the regulation of antigen-specific IgE production, accumulation of eosinophils, and activation of mast cells. In this connection, the incidence of allergic disease and atopy has markedly increased in the industrialized countries compared with developing countries over the past decades, and one hypothesis is that this increase is linked to the reduction  of bacterial infections, which occurs in a cleaner  environtment, a hypothesis known as the “hygiene hypothesis “. The discovery that TLR signaling  might be crucially involved in the establishment of TH1/TH2 pathways opens up the field to look for new strategies against diseases such as asthma and atopy

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2 Responses to Immunological aspects of infections part 12

  1. This may be one of those anecdotes that interest only the speaker and his mother, BUT –
    I’ll never forget how, well, impressed, I was last year by the bacterial strain that transformed my left thumb (via a TINY cut) into a huge, inflated, bright red sac that jumped with surges of pain at the very slightest touch. This bacteria brilliantly resisted all three major (commercial) topical antibiotics for two full months! And this happened after a lifetime of NEVER getting infections when everyone around me was dropping (figuratively) like flies. Finally, my own army vanquished the invader (unless those topical antibiotics can triumph after two months?)
    I wonder if that wasn’t a new or particularly resistant strain at all. Since I never got infections, do you think all those decades with no pathogens alerting the production of those cytokines eventually weakened my famous immune system? In that case, was my immune system generally strengthened by its prolonged and finally successful resistance? Like, it finally got a work out after a lifetime of sitting around doing nothing?
    Thanks for considering this. My apologies if my story is a common one (it’s certainly a long one) and/or my question is dumb.

    Good blog!

    Liked by 1 person

  2. azaleaazelia says:

    Your left thumb (via a tiny cut) was port the entry for the bacteria. It got infected with the inflammation signs (transformed into huge, inflated, bright red sac that jumped with surges of pain at the very slightest touch). Your immune system worked properly but still need medicine (antibiotics) to resolve them. Sometimes you need oral antibiotics to resolve the bacteria, not just topical antibiotics.

    Liked by 1 person

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