And as a B cell matures, it develops the ability to determine friend from foe, developing both immunocompetence -- or how to recognize and bind to a particular antigen -- as well as self-tolerance, or knowing how to NOT attack your body’s own cells. Once it’s fully mature, a B lymphocyte displays at least 10,000 special protein receptors on its surface -- these are its membrane-bound antibodies. All B lymphocytes have them, but the cool thing is, every individual lymphocyte has its own unique antibodies, each of which is ready to identify and bind to a particular kind of antigen. That means that, with all of your B lymphocytes together, it’s like having 2 billion keys on your immune system’s keychain, each of which can only open one door.

This is what Hank said in Crash course. So the b cells, each are having several unique antibodies and I also saw that this is true for T cells too and the dendritic cells look for a helper T cell that can bind the parts of the intruders which the dendritic cell has presented on its membrane.

my question is

What if there is no antibody in any cell against an antigen?

Does the immune system has antibodies against all antigens in the world?

What happens if an antigen came into our body which has no antibody matching for it?

  • $\begingroup$ A clarification: each individual B cell has only one type of antibody. They can have many thousands of copies of it, but the copies are all identical. $\endgroup$ – MattDMo Jan 15 '17 at 23:43
  • $\begingroup$ @Matt this information is very useful for me. thank you for the clarification $\endgroup$ – cumulonimbus Jan 16 '17 at 3:35
  • $\begingroup$ No problem. Incidentally, T cells are the same way - they have tons of T cell receptor (TCR) complexes on their cell surface, but all have exactly the same sequence, and are specific for exactly the same antigen. Now, as Joe Healey points out below, there can be cross-reactivity between antigens (sometimes substantial cross-reactivity, something he doesn't mention), which is the basis of a polyclonal immune response. $\endgroup$ – MattDMo Jan 16 '17 at 15:02
  • $\begingroup$ @Matt All the comments and answers are really a learning curve for me.I learned a lot like v(d)j gene, cross reactivity, polyclonal response. So thank you very much. $\endgroup$ – cumulonimbus Jan 17 '17 at 10:16
  • $\begingroup$ Most likely, another antibiody matching another antigen from the same infectious source takes care of it. $\endgroup$ – Joshua Jul 10 '17 at 21:00

The same thing that happens to the native american when they were first exposed to smallpox. Extermination of 90%-95% of the population. https://en.wikipedia.org/wiki/History_of_smallpox

The immune system is unable to attack bacteria or virus which makes unrecognizable antigen. As a result the bacteria/virus continue to grow and grow unopposed, until the person dies.

The disease goes wild, spreads like wild fire, killing every single individual it infects. In the worst case scenario, the species may go extinct.

EDIT Why do vaccines work. Firstly the adaptive immune system is adaptive. The immune system generates new antibodies (ie new keys) by splicing together different version of the V(D)J genes in a big round of mixing and matching. Then it uses an enzyme called AID to induce hypermutation to that combination. The end result is a nearly limitless number of antibodies (keys).
https://en.wikipedia.org/wiki/Somatic_hypermutation https://en.wikipedia.org/wiki/Antibody

However this process takes time. And during that time the bacteria/virus is growing and growing. Weakening the body. So it becomes a race. Can the body generate an antibody that recognizes the bacteria/virus, before the body dies.

A vaccine helps in this respect, because the vaccine is can expose the immune system to the antigen of the deadly virus/bacteria without actually using the active/live virus.

ie Some vaccines only uses pieces and parts of the bacteria/virus. The antigen is there. But the virus is dead.

In other older vaccines, the virus used in the vaccine has been weaken/mutated so much that it has a low probability of beating the body before the immune system. https://en.wikipedia.org/wiki/Edward_Jenner

In the Edward Jenner cowpox vaccine... the cowpox virus so happened to have antigens similar enough to smallpox, that antibodies against cowpox works on smallpox. And cowpox is not deadly to humans.

Now.. here is the interesting part. The arms race between host and disease has gone on for a very long time. So many viruses develop what is equivalent to chaff. These are proteins that stick out on the membrane surface and thus easily recognized by the immune system, but are rapidly changed. So by the time the immune system launches an aggressive response, the protein changes again. Kind like a disguise that a thief changed every time he robs a bank, so the police are always one step behind. The bacteria grows and grow. Constantly switching its antigen coat and eventually the person dies.



A vaccine in this case, presents the immune system with the one part of the bacteria antigen coat that does not change. So an effective immune response can be made. However as experience with HIV antibodies has found, those constant parts tend to be protected by the parts that do rapidly change. So antibodies have trouble reaching it. And this is why we do not have vaccines for HIV. The constant regions are too well protected.

One response to this can be seen in flu vaccine. Here the virus changes it antigen coat not every few days, but on average once a year. So we try to predict what is the flu strain of the year.. and raise a vaccine to the antigens of the year. Sometimes the predictions are spot on, so the vaccine works perfectly. Sometimes the antigen predictions are a little off... so the vaccines don't work so well. And on a rare bad year, the predictions are completely off. And the flu vaccine do not work.

  • $\begingroup$ That's a great answer. I never read anywhere about production of new antibodies for new antigens. So I doubted how then we survived several diseases which are always evolving. you cleared it greatly.thank you for adding additional informations. thank you very much. $\endgroup$ – cumulonimbus Jan 16 '17 at 6:59
  • $\begingroup$ All the comments and answers are really a learning curve for me.I learned a lot like v(d)j gene, cross reactivity, polyclonal response. So thank you very much. $\endgroup$ – cumulonimbus Jan 17 '17 at 10:16

The Native Americans and smallpox

First I want to note that some of the posted answers are not quite accurate. For example, smallpox ravaged the Native American population because they did not have high-affinity MHC molecules for it, which is an evolved trait. MHC molecules must be capable of binding to a large class of peptides, at least weakly, to allow their presentation. There are only a finite number of MHC alleles in a given individual, and they tend to represent the most commonly found classes of foreign organisms.

The Native Americans were equally capable of creating anti-smallpox antibodies as any European, but that process was significantly slowed down due to not having MHC alleles which promote the presentation of smallpox, allowing the virus to accumulate to lethal levels before a sufficiently mature immune response could be mounted. You can bet that the survivors were the ones with MHC alleles that promoted rapid recognition of the virus!

Somatic hypermutation and affinity maturation

The way antibodies work is, B cells undergo both genetic recombination and an intentionally increased mutation rate called somatic hypermutation. This results in a virtually uniform distribution of new antibodies. These new antibodies are actually pretty bad at binding antigens, and at best, only roughly approximate them. This is one reason the first exposure takes so long to eradicate. When an antibody that weakly matches is found and the number of B cells rise, some of them begin to induce additional mutations to their antibody, a process called affinity maturation. The mutations that result in breaking the antibody end up discarded (those B cells die), whereas those that have an even stronger affinity result in the clone of B cells being positively selected for. This goes on and on until the resulting clone of B cells produce extremely high-affinity antigens.

The result of this is that virtually any possible "door" will have a "key", even if it is poorly fitting. Over time (and subsequent exposures), the key is fine-tuned. The only way a persistent antigen could evade an immune response, short of interfering with the immune system is if the antigen is extremely similar or identical to a self-antigen.

Some pathogens can avoid an immune response in indirect ways, such as frequently changing exposed antigens either by switching genes or through rapid mutation, covering the cell surface with self-antigens or innate, non-protein material, tucking conserved regions that act as epitopes deeply inside a protein, releasing molecules that inhibit the immune response, etc.

Foreign antigens resulting in production of anti-self antigens

An interesting thing to note is that, even if the antigen is similar to self, it will still often be detected. This can be highly problematic because selection against anti-self antibodies occurs when the B cell is first developing, during somatic hypermutation, but not during affinity maturation. A weakly binding antigen that is similar to a self-antigen may then stimulate the production of anti-self antibodies since the antigen is different enough from self that B cells specific to it are not negatively selected, but similar enough to self that the changes in affinity maturation are sufficient to convert it into an anti-self antigen (in other words, an antibody x steps away from targeting self-antigens results in negative selection, but affinity maturation results in y changes to the antibody, where y > x). This is one reason why some viruses can trigger auto-immune diseases.

Answering your questions directly

What if there is no antibody in any cell against an antigen?

If for some reason no antibody were even had the slightest affinity for an antigen, then there would be no problem, and a pathogen would trigger an immune response because of another antigen. If for some insane reason every single antigen on a pathogen (there are many) was not even slightly matched, then no humoral immune will be invoked. There still may be a cellular immune response (e.g. for viruses), and the innate immune system would still be active.

Does the immune system has antibodies against all antigens in the world?

The immune system has antibodies that bind a wide range of antigens, albeit weakly, and with high overlap. As a result, you could say that all possible antigens that are not too similar to self are countered by antibodies with at least some level of affinity. There is only a finite number of possible antigenic peptides, and of those, all that's needed is a weak interaction to trigger a full-blown adaptive immune response.

It's like going to an ophthalmologist. They don't have lenses for all possible refractive indexes, but they do have enough samples that, by trying them out, you can see which ones improve your vision. Going through this process allows gradual improvement, and eventually they are able to proscribe a perfect match.

What happens if an antigen came into our body which has no antibody matching for it?

A single antigen, as opposed to a pathogen with many antigens? Ignoring the cellular immune system, nothing would happen. It would be treated virtually identical to self-antigens (i.e. it would be ignored). Depending on how the pathogen behaves, it could be wiped out by the rest of our immune system, contained in a local cyst, or even result in a lethal infection.


If you have no antibody to a particular antigen, you have no immunity to that molecular pattern (and the organism it belongs to).

That's the basis of immunity.

This is why you have vaccinations. You are artificially exposed to an antigen your immune system hasn't seen before, so you sero-convert and then have immunity.

That passage is a little misleading though, its not quite one key-one lock, as it's possible for antigens to have slight crossreactivity (which is why you can be vaccinated against one thing, with a related thing (e.g. the old Jenner cowpox vs smallpox example).

  • $\begingroup$ Thank you for adding information like cross reactivity. I thought the same as in your answer i.e. we will die if we dont have any antibody against an antigen. But I cant understand sero conversion. I saw in Wikipedia and they said it is the time period during which a specific antibody develops and becomes detectable in the blood. I read it fully and understood what sero conversion is. But how is this is related to your answer. And if our immune system produce antibodies for vaccines why can't it directly produce antibodies for new antigens that enters our body? Thank you for the timely help. $\endgroup$ – cumulonimbus Jan 16 '17 at 3:47
  • $\begingroup$ You mix up two things: If there is no antibody, there is no immunity. And there will be none. If you vaccinate, you have at least low affinity antibodies, which are then adapted to fit better. This happens during infection, but this takes some time (around two weeks until full production of new antibodies, which might be too long for some diseases). Immunisations short-cut these time, as they mimic the infection and give the body the time to produce the necessary high affinity antibodies without being terrible sick. $\endgroup$ – Chris Jan 16 '17 at 6:03
  • $\begingroup$ @Chris The comment that you wrote, Is it for cumulonimbus(me) or for Joe Healey? $\endgroup$ – cumulonimbus Jan 16 '17 at 6:52
  • $\begingroup$ @cumulonimbus It is to Joe's answer. $\endgroup$ – Chris Jan 16 '17 at 8:54
  • $\begingroup$ @Chris You're saying I'm mixing up 2 things? I don't see how? Your comment says exactly the same thing my answer did. $\endgroup$ – Joe Healey Jan 16 '17 at 9:05

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