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The king of sterile immune response is antibodies; while in unsterile response - T lymphocyte. I think there can be two types of IRS: either abnormalities with T or B cells. Assume the here the case is abnormalities with B cells. This is the reason why sterile immune response is called paradoxical in IRS:

  • there is an abnormality with B cells here in IRS
  • sterile immune response is mediated by low level of B cells

but still this combination can lead to the effective secretion of antibodies in local sites resulting in sterile immune response.

APC cells present antigen to antibodies. Then, the B cells (together with the T cells) can check these. B cells need to receive the correct co-stimulatory signal. Neither of them plays alone, they are usually connected in many ways. If antibodies are foreign, you start making antibodies.

Sterile immune response expresses locally free area of specific microorganisms i.e. antigens are unique causing production of unique antibodies. The response has complete immunogenicity i.e. the ability to cause immune response. There are more than one epitope on the antigen with which antibodies can react. Specific antigens are antigenic i.e. antigens can react with antibodies. They can be thymus dependent i.e. proteins (species specific, may be the case if immune response is virus related), but also m/o polysaccharides (m/o type specific, not viruses here, only bacterial and fungal). They expresses IgM, but surprisingly, very weak immunological memory (IgG).

Antibodies are the antigen-specific products of B-cells. The production of antibodies to infection is main part of adaptive immunity. Antibodies are plasma proteins (immunoglobulins). AB of sterile IR binds specifically to molecules from the pathogen ($F_{ab}$). They do recruit other cells to destroy the pathogen ($F_c$), which is dominant in the sterile immune response here.

Immune Reconstitution disease is coupled by prolonged hypersensitivity I reactions. Assume the site of such allergy prolonged IRS state is upper respiratory tract. However, the sterile immune response reaches local proximities i.e. also limb extremities, nose and ears. There is lower activity of phagocytosis so the process against the initial stage of infection is ineffective (specific immune response).

My conjuncture: The body has developed alternative pathway against infections. This is done by sterile immune responses.

However, I understand very little about how these sterile immune responses are regulated. There are many factors 1) Microbial (opsonins), 2) Human organism (histamine, Ca2+, Mg2+) - also open factors (avitaminosis, stress, sleeplessness, ...).

So the phagocytosis activity is lowered. However, its effectiveness locally seems to increase i.e. sterile immune responses.

My conjuncture for this is increased sympaticus to increase the content of some glandular secretions (not of all glands; there is one type of glands which activity is decreased by sympaticus). There can also be a mechanism through a baroreceptor reflex arch to alter the flow of such sterile responses in short term.

There are many mechanisms which can start such sterile immune response. I know very little about them. Possible mechanisms of activating Sterile immune response in non-IRS

  • Clear antigen (e/c, allergen) presentation by dendritic cells to non-naive T cells; and Proliferation, differentiation into effector cells. Cytotoxic antibody production.

Possible mechanisms of activating Sterile immune response in IRS

  • Cross Antigen (e/c) presentation by dendritic cells to naive CD8+ T cells; activation of 2nd signal - costimulation B7-CD28; activation of 3rd signal - cytokines IL-2 released by Th1. Activation of naive T cytokines: Proliferation, differentiation and cytotoxic antibody production $\to$ $F_{as}$ receptor on surface of lymphoid and nonlymphoid cells $\to$ transmits apoptosis signal $\to$ infected cell dies.

Open are

  • the mechanisms of action of Tcyt
  • not sure how viral immunity is the case here. If virus related immune response, then interferons (IFN-alpha, leucocyte interferon and allergens) participate in IR inhibiting the viral replication.

This process is against pathogens (normally viruses; but here prolonged exposure of allergens) that do not readily infect antigen-presenting cells, or impair dendritic cell normal function.

Scheme of Sterile immune response in IRS

  • Allergens presented by APC to B/T cells induce the antiviral state within a few hours of interferon stimulation. Assume this state is continuous, since it relapses all the time more and more; each cycle lasting 1-2 days. I am not sure about the specific state here.
  • Allergy - mediator low quantity of IgE in hypersensitivity I. I am not completely convinced that Allergy refers anymore only to hypersensitivity I here in IRS because normally the second contact with allergen leads to altered reactivity. It is possible that this altered reactivity in the first contact or no alteration occurs.
  • Other mediators also because of IRS.
  • In this state, the sterile immune response can then be induced somehow.

So the characteristics of Sterile immune response is similar to anaphylactic shock in some ways

  • specific (local areas)
  • immediate reaction
  • antibody IgE (not sure how in IRS), some IgG (probably IgG4 only)
  • Possible atopy (increased susceptibility to IgE antibodies) which function in IRS is unknown.
  • no anaphylaxis
  • dose and route of allergen determines normally the type of IgE-mediated allergic reaction, but this is open here

How are the sterile immune responses fine-regulated in the short term? I have not found any evidence that they can be prolonged.

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What do you mean by sterile immune reaction? To make antibodies, B cells need to receive the correct co-stimulatory signal. Neither of them plays alone, they are usually connected in many ways. Although this is something what many people do not see. –  Chris Jun 6 at 17:25
@Chris Sterile immune response expresses locally free area of specific microorganisms. –  Masi Jun 7 at 7:09
Sorry, but I still don't understand. You need contact with antigens - which are then presented by antigen presenting cells. Then the B cells (together with the T cells) can check these. If they are foreign, you start making antibodies. –  Chris Jun 7 at 8:33
@Chris Yes, you are right. That is the basis about the topic. I am interested in the fine-regulation of the sterile immune responses. How can they be possible for short term? The antigen can be the polysaccharide of microorganism, for instance; here allergen. –  Masi Jun 7 at 9:47

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