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the macrophages are pretty known well for antigen presenting process and to present the antigens which are bound to pathogens unlike exotoxins (which are free) the pathogen first should be digested and destructed and derive the antigenic portion and present it to T cells then stimulate the B cells to make antibodies. If the macrophages can destruct and digest the pathogen to derive the exact antigenic portion so then whats the need of humoral immunity to be activated because they have already destruct and kill the pathogen if your answer is that the pathogen gets knocked out quickly by antibodies for the second if they invade,so there are millions of other infecting agents every day invading our body and are omitted by the first line defenses?

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  • $\begingroup$ To answer your question properly would pretty much require giving an entire semester's course in immunology. As there isn't the time or space to do this here, my suggestion would be for you to read Janeway's Immunobiology This is the 5th edition, and from 2001 is likely very stale, as the current version is the 8th edition, and there have been many advances in immunology in the last decade and a half, but it is a start to your answer and will give you a better grounding. $\endgroup$ – AMR Oct 7 '15 at 4:01
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Let's consider some situations real quick:

(1) A bacterial microbe enters through a fissure in the skin. What does an innate, systemic immune response look like? In short: it's lengthy, uncoordinated and has a lot of potential to damage tissue in the area of infection.

(2) A bacterial microbe enters the blood. The bacterium produces an AB toxin that enters cells and kill them.

(3) The host is infected by a helminth.

In situation 1: Innate immune responses are associated with the secretion of many cytokines and chemokines. Cytokines are associated with the inflammatory response, and chemokines are associated with lymphocyte trafficking. Inflammation and recruitment of lymphocytes, macrophages and the like are good for clearing the infection, but there's a lot of potential to damage the surrounding tissue. Effector cells from the adaptive response incl. humoral immunity don't elicit the same level of damage, and we can illustrate this in mucosal immunity. Since commensal (and some pathogenic) organisms are constantly stimulating mucosal immunity, there are (1) epithelial effector T cells, (2) plasma cells and (3) dendritic cells that make the response to these pathogens fast, efficient and little damage occurs to the tissue involved.

In situation 2: So let's say the pathogen has escaped the immune response, maybe it's encapsulated. There are AB toxins being produced that kill cells endocytosing them. What good will it do for a phagocyte to eat something that ends up killing it? Antibodies are particularly efficient for this extent because they can neutralize toxins they've encountered with the same fast, efficient response as we described above. This is achieved through antigen presentation. The host will then need to find other ways to clear the infection, however.

So: In situation 1 we illustrated that an innate, systemic response isn't always desirable due to tissue damage, and through the presentation to T cells by APCs, a later adaptive immune response mitigates this effect through formation of effector cells. In situation 2, we then illustrated that the first-line defenses can't always respond to the imminent threat for various reasons, which are overcome by the presence of effector cells.

Situation 3: This is the more complex concept. You have different subsets of CD4+ T cells that can be formed in response to the type of interleukin or cytokine that is present when the CD4+ T cells are being activated. This differentiation is driven largely by secretions of activated APCs! The APC performs this critical step based on what kind of receptors the specific types of pathogen are detected by. The differentiated CD4+ T cells, or T-helper cells of class: Th1, Th2, Th17, Treg, etc. each perform different roles which are effective in different situations. For example, you wouldn't see any benefit in throwing Th1 cells at a helminth infection, Th2 is the best effector for this. Treg cells are capable of abrogating autoreactivity, and Th17 cells are needed to assist B cell differentiation in response to antigen detection (which in the case of helminths, the B cell must class switch to IgE and this is stimulated by Th2 cells via IL-4).

Now, in situation 3, we've illustrated that CD4+ T cell intermediates are providing your overall immune response: flexibility, specificity, and checks/balances which are all-at-once critical to healthy functioning. I disregarded MHC-I responses and CD8+ CTL's because this is about APC-driven responses.

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  • $\begingroup$ I did my best to provide something robust without going into deep detail, if anyone has a problem with the content let me know! $\endgroup$ – CKM Dec 5 '15 at 21:48
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In nature and biology, the question of 'why something happens' is difficult to answer. Because, biological processes are 'not designed' to address a deficiency or fulfill be a need of the organism. On the contrary, biochemical processes undergo changes (induced or otherwise) leading to a number of new related processes which may confer advantages in altered environments. Therefore, to accomplish a task, every organism may use multiple pathways.

Eliminating a foreign molecule or an agent, is generally accomplished by a co-operative action of innate and adaptive mechanisms of immune system. Although innate mechanisms often can control propagation of some foreign agents, adaptive immunity and subsequent memory mechanisms of B and T cells are fast acting in subsequent exposures of many agents.

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  • $\begingroup$ I'm not really sure this directly answers the question. It gets to the issue of asking "why", I suppose, but that might be better phrased as a comment. $\endgroup$ – Amory Oct 6 '15 at 18:15

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