Leprosy and TH1 vs TH2

[MudPhud20XX]

Alright, so I am finally done with Kaplan neuro! Thank you all for your help in neuroanatomy!

Now I started Kaplan immuno and have some questions:

So Kaplan explains Tuberculoid Vs. Lepromatous Leprosy as below:

1. Tuberculoid leprosy: strong TH1 response
2. Lepromatous leprosy: strong TH2 response & reciprocal inhibiton of TH1

So I get the idea that Leprosy is due to the bug Mycobacterium which is the intracellular pathogen so that it turns on TH1 response, but then how the heck do you get strong TH2 response in case of Lepromatous leprosy? I mean these two types of leprosy must be due to the same bug right?

Also, during the video lecture, Kaplan says more severe form is the "Lepromatous leprosy." Does it have to do with the fact that it suppresses TH1 response so that you get more severe symptoms compared to "Tuberculoid leprosy?"

Has anyone seen any relevant UW question with regard to this topic?

Many thanks in advance.

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[notbobtrustme]

The bug itself can influence whether or not you have Th2 response or not. It all depends on your genetics. Some people can fight the bug's influence, some people can't.

 

[Fatalis]

there are a couple of UW questions on this. You get the TH2 response if the patient has a compromised TH1 function; think of it as a compensatory mechanism.

 

[ninjasurgeron]

Based on current research, its mainly genetics. Some people are susceptible to infection and most are not. Think of tuberculoid and lepromatous leprosy as the outcome of the body's response to infection.

If your body responds effectively, i.e. TH1/cell-mediated response to an intracellular pathogen = tuberculoid/paucibacilliary
If it throws antibodies at an intracellular microorganism = lepromatous/multibacilliary

It helps to know older/alternative names to diseases as they usually give as to how to remember a disease.

 

[alicealicealice]

The different clinical manifestations of tuberculoid vs lepromatous leprosy has to do with host genetic factors rather than pathogen factors. Some people are not susceptible at all (<1% of people are susceptible), some get tuberculoid, some get lepromatous all in response the the same genetic form of the same bug.
Why that is is multifactorial, but it has mostly to do with the genetics of the hosts immune response that predispose them to Th2 over Th1 response when exposed to the bacterium (but also environmental factors like nutrition, vacc status, size of innoculum). Fatalis is right as these people have a "compromised Th1 function", but its not like they have AIDs or a classic immunodefiency syndrome; its more like a genetic vulnerability that gets revealed in the presence of a specific environmental trigger (in this case, infection with M.leprae).
www.lepra.org.uk/platforms/lepra/files/lr/Sept06/Lep189-202.pdf

 

[Fatalis]

these people have a "compromised Th1 function", but its not like they have AIDs or a classic immunodefiency syndrome; its more like a genetic vulnerability that gets revealed in the presence of a specific environmental trigger (in this case, infection with M.leprae)

I should have made that distinction when I said immunocompromised, good catch!

 

[alicealicealice]

np, what you said is still right. also worth menionting as UW does that in real life as to be expected its a spectrum, people usually present with a phenotype somewhere in between.