From Article: A little of Immunology for Everyone and Autoimmune Diseases
By Dr. Hector Jara - Neuropharmacologist, Researcher in clinical neuroimmunology.

Immunology is the science responsible for studying the ability of our body to defend ourselves from any kind of invasion, be it: bacteria, fungi, viruses or cancer. On the other hand, it studies the phenomena related to autoimmunity, which consists of a self-attack of our defences towards our body. It is like the dog in your house attacking you, its owner, thinking it’s the thief. This last phenomenon is the one that I am going to develop in this chapter in order to understand a little more about the relationship between stress, depression and immunity.

Immunity is mainly exerted by lymphocytes which are a type of white cell (leukocytes or white blood cells). Other blood cells act in the immunity system (the so-called innate immunity), but these are the most important:

What are the defences of our body? – TH1 and TH2 immunity

There are two types of immunities to explain the autoimmunity phenomenon: Th1 immunity and Th2 immunity. They used to be called cellular immunity and humoral immunity, respectively. There is immunity th0, which is the real point of balance since it behaves like th1 and like th2.


TH1 IMMUNITY is in charge of defending us with T-lymphocytes against viruses, fungi and cancer cells (when it detects invaders, it destroys them). It also helps in the attack against bacteria, but it is not its primary duty. In this immunity, the lymphocytes produce substances that destroy the aggressors. These lymphocytes are called cytokines, interleukins or substances with the ability to damage a fungus, virus or cell detected as foreign to our body.

The most important cytokines of the TH1 immunity are interleukin 2, tumour necrotizing factor (TNF) and interferon-gamma. It has been shown that many autoimmune diseases are related to an increase in this immunity, which for genetic reasons, among others, that I will mention later, can destroy different types of organs or tissues. Thus the medical literature reports many TH1 diseases such as psoriasis, multiple sclerosis, Crohn disease, autoimmune hepatitis, thyroiditis and their consequences such as hypothyroidism, rheumatoid arthritis, alopecia areata, Sjogren’s syndrome, rheumatic fibromyalgia, myasthenia gravis, hodgkin lymphoma, contact dermatitis, autoimmune pancreatitis, frequent abortions, sarcoidosis, vasculitis in general, nephrotic syndrome, bronchial asthma and insulin-dependent diabetes mellitus.

Various studies demonstrate these findings; they consist of measuring interleukins in damaged tissue as well as lymphocytes with TH1 or TH2 capacity in the blood. The important thing is to know that this type of immunity, despite protecting us against fungi, viruses, intracellular parasites and cancer cells, at a given moment polarises or is predominant over th2 immunity and could damage our own tissues.

When reviewing the literature on the subject of neuroimmunology, there is considerable evidence that shows the relationship between depression and autoimmune diseases Th1. Depression, from the neurochemical point of view, consists of depletion of cerebral serotonin (of the dorsal raphe) and an increase of cerebral norepinephrine (of the A5 nucleus).

Excess norepinephrine can be detected in the blood. This substance activates the thymus, which is a lymphoid organ found in the thorax responsible for training lymphocytes to increase their Th1 activity. For this reason, depression is associated with th1 autoimmunity or vice versa.

Not all depressed individuals will suffer from Th1 autoimmunity, but almost all Th1 autoimmunities present the neurochemical profile of depression. There are also receptors for norepinephrine in other lymphoid organs and in the lymphocytes themselves, which causes them to polarize towards th1 when this neurotransmitter increases in the blood.

Obesity causes th1 autoimmunity in most obese patients because excess fat behaves like a th1 interleukin-producing gland. That is why metabolic syndrome has a relationship with depression and hypothyroidism.


The TH2 IMMUNITY also consists of a self-attack on our tissues, but it is not directly the lymphocyte that attacks. It is an attack through antibodies (which are those that increase with vaccines) or the so-called Immunoglobulins (the IgG that increases to prevent the infection from recurring and the IgM that increases in acute infection). These antibodies are produced by B-lymphocytes. B-lymphocytes are more closely related to stress. They increase when there is stress. When there’s stress, they are like the front line defence.

This Th2 immunity, which is that of B-lymphocytes and which attacks almost everything with little immune memory, is responsible for allergies, which are inflammatory reactions that appear very quickly. B-lymphocytes have receptors that, thanks to their great diversity, can recognize any foreign material –a logical response from nature. When we are in front of an aggressor (stressor), it is normal for the immunity to increase and protects us, by attacking everything it finds (for example dog saliva, a predator or a rusty knife). It uses first-line warrior cells that attack with the help of other cells like mast cells and eosinophils; which discharge a series of substances that can be toxic to bacteria and inflame tissues: histamine, serotonin, th2 interleukins, etc.

IgE is generally elevated and contributes to the response described. We have been able to observe that a stressed patient may have Th2 autoimmune disease or may have diseases related to low Th1 immunity: cancer, frequent viral infections, infections caused by intracellular germs (mycoplasma, TBC), frequent fungal infections (for example reoccurring vaginal yeast infection).

The most frequent Th2 diseases are allergies of all kinds, atopic dermatitis, respiratory allergies, chronic rhinitis, Ulcerative Rectocolitis, gastritis or eosinophilic colitis, etc.

T and B lymphocytes that do not transform into Th1 and Th2 effector cells will persist for a long time as immune memory cells. With a new stimulus of the antigen, a specific immune response will take place (they have already recognized the antigen once) and they will produce a greater amount of antibodies (because they are more numerous). This is the mechanism that explains the success of vaccines: The individual receives the dead or attenuated germ in the vaccine and establishes a first response (the discomfort of vaccines at the beginning with fever). Later, when the infection occurs, the memory cells are quickly activated and eliminate the aggressor.

In summary, Th1 immunity is related to depression and protects us from cancer. Th2 immunity is related to stress and protects us little against cancer. In other chapters I will describe each type of autoimmune disease and the neuroimmune treatment.

Treatments of autoimmune diseases

Unfortunately, current treatments are aimed at immunosuppressing patients with this type of disease. Steroids are generally used as a first-line drug. All types of immunosuppressants are tried, such as methotrexate and other chemotherapeutic agents that generally produce many side effects. As the saying goes “The remedy is worse than the disease.”

I believe that steroids can be used when the disease is very aggressive or affects a vital organ, but it should only be used for the first few days or for a short time.

Steroids have their place in medicine but cannot be prescribed for long periods of time and in high doses. The danger of these drugs when used for long periods of time is that in addition to producing hypocarticalism (our ability to produce cortisol disappears) and other diseases (hypertension, diabetes, steroid psychosis, acne, Cushing’s syndrome, severe osteoporosis, growth retardation, infections a recurrence, necrosis of the femur head, cataracts, etc.), patients generally die from the chronic effect of the treatment and not from the disease. Other immunosuppressants, such as tacrolimus and cyclophosphamide, have been linked to severe infections and cancer.

Lately, genetic engineering drugs have been produced to avoid the use of steroids. They are destined to block the effect of interleukins by blocking the receptor on where they act: The necrotizing tumour factor (inflimibax) and IgE blockers.

I believe that these treatments always lead patients to immunosuppression and make them susceptible to infectious diseases and cancer. I am not in favour of applying this type of treatment to autoimmune patients. There are already case reports of fatal infectious diseases due to the use of these drugs, and the pharmaceutical industry defends the use of the drug, arguing they did not see this effect in their multicenter studies.

Neuroimmune treatment consists of verifying the existence of stress or depression and whether it is possible to classify the patient as Th1 or Th2 to start a neuropharmacological treatment that reverses the predominant condition. When the patient has been treated long-term with steroids, the results are not so encouraging. There is a good response in Rheumatic Fibromyalgia (many patients cured), Multiple Sclerosis (especially if the patient comes in the first crises), Myasthenia Gravis (Without thymectomy they respond much better), Rheumatoid arthritis (sometimes we use treatment with very low doses of methotrexate), Bronchial Asthma in children, Allergies, Crhon disease, Ulcerative Rectocolitis, Sjogren’s Syndrome, Alopecia, Pemphigoid, Autoimmunity, Hepatitis C and autoimmune hepatitis.

Psoriasis, Vitiligo and Systemic Lupus Erythematosus are the three autoimmune diseases that are most resistant to neuroimmune treatment.

Source: Dr. Hector Jara – Neuropharmacologist, Researcher in clinical neuroimmunology.
(Translated from the original Spanish