An Immune Response in any individual, with or without a specific disease, simply refers to the body reacting to a foreign agent. Occasionally the body goes haywire and starts to react against its own tissues. This is called an AutoImmune Response.
The host's Immune System may be involved in the onset or perpetuation of MS. Cells of Lymphoid Tissue (Thymus, Spleen, Lymph Nodes, & certain blood cells) generate and control an Immune Response.
In humans, most of the information has been obtained from studies of Lymphocytes (certain blood cells), which are readily accessible for analysis. These Lymphocytes may be subdivided into different types, which have several specialized functions.
Some (B-Cells) produce and secrete AntiBody. Other Lymphocytes (T-Cells) directly attack and destroy an infectious organism; these are "effector" T-Cells. Other T-Cells help promote an Immune Response or suppress it; these
are "Regulatory" T-Cells.
Investigation of the general Immune status of MSers has disclosed no consistent abnormality in the blood, although when more specific and sensitive tests are used, regulatory Lymphocytes of the T-Suppressor type sometimes have been found to be reduced in number or actions.
That is, there may be a decrease or disappearance of these Lymphocytes from the peripheral blood, or a decline in their function at the very time MS exacerbates. The function of these cells returns to normal or above normal when the patient goes into remission.
Whether these cells are destroyed, enter the CNS, or merely alter their circulatory route in the body remains to be determined. The Lymphocytes in MS plaques include B & T-Lymphocytes without a selective T-Cell type (Helper or Suppressor) dominant.
It is also unclear how an alteration of the number of regulatory T-Lymphocytes would manifest as MS, but the correlation some times noted of the cyclic changes in clinical symptoms and the number of these cells in the bloodstream is intriguing.
It has been known for more than 35 years that there is usually an increase in the amount of ImmunoGlobulin in the CerebroSpinal Fluid of MSers'.
IgG is the predominant ImmunoGlobulin. CerebroSpinal Fluid normally has up to 45 milligrams of protein per 100 milliliters; IgG constitutes less than 15% of the total amount of Protein present.
As noted, in MSers, the IgG in the CerebroSpinal Fluid is increased, primarily because of the production of IgG by certain cells (Plasma Cells) within the CNS.
These cells appear to arise from blood Lymphocytes, which enter the CNS when the MSer is having bouts of inflammatory Myelin damage.
When examined by suitable techniques, the CerebroSpinal Fluid Proteins of the vast majority (80 to 90%) of MSers show selective increases of certain forms of IgG, but the presence of these forms of IgG in CerebroSpinal Fluid is not specific for MS; they are also found in other diseases as well.
In association with the changes in IgG in the CerebroSpinal Fluid, AntiBodies to a number of Viruses are also found to be increased.
However, neither of these conditions is specific for MS or even precisely parallels the disease's activity. The activity of the major parts of the IgG in CerebroSpinal Fluid is unknown. Attempts to determine this activity are currently being made in many reasearch
Viruses And Multiple Sclerosis
Viruses or other infectious agents have been suspected for many years to be the cause of MS. As different infectious organisms have been discovered and identified, they have been examined for a possible linkage to MS.
During the past 20 years, attention to an infectious basis for MS has been directed primarily at Viruses.
Numerous types of Virus exist with an array of features that determine how they infect and alter tissue. The behavior of the Virus is the result of a Virus's own characteristics and the cells to which it is exposed.
A host cell may show a number of reactions in response to a Viral infection, ranging from minimal or no change to malignant transformation to death.
In addition to the changes produced by the usual type of Virus, mutant Viruses may appear that have different characteristics of infectivity or disease induction.
Evidence for Viral involvement in MS or any condition can be sought using several methods. The most convincing is the culture, isolation, and identification of a Virus in tissue taken from areas of damage.
Other methods include recognizing parts of a Virus in tissue and detecting AntiBodies (which would attack that particular Virus) in the blood or CerebroSpinal Fluid of those affected. Finding the AntiBody would indicate that the person had been exposed to the Virus at one time or another.
The Virus that causes Measles has been analyzed extensively as a possible cause of MS. This Measles Virus is known also to cause a chronic Nervous System disease of childhood called Subacute Sclerosing PanenCephalitis.
Beginning in 1962, it was recognized that persons with MS have increased amounts of AntiBody to the Measles Virus in their bloodstream.
Although a number of studies have confirmed this observation and have also shown that some of the AntiBody to Measles is being produced by the CNS, evidence for the Measles
Virus also causing MS remains highly circumstantial.
When attempting to relate enviromental influences from 10 to 20 years before, to the appearance of MS now, a "Slow Virus" must be considered.
In contrast to the usual acute or subacute response to conventual Viruses, "Slow Viruses" cause disease that may evolve over a period of months or years.
One of these Viruses induces an inflammatory CNS disease in sheep, but there is no
indication that any one of the known "Slow Viruses" causes MS.
Several conventional Viruses have been identified as causing a CNS disease in animals that shows some of the same tissue changes as are seen in MS.
Hence, because of the many mechanisms whereby a Virus might inflict CNS damage, a Viral Etiology for MS has by no means been excluded.
Although some helpful diagnostic procedures and tests have been developed, the diagnosis of Multiple Sclerosis is still based on the history and Neurological examination.
The physician must be able to show that there are two or more areas of lesions in the
Central Nervous System (CNS) - the Brain and the Spinal Cord.
There must be evidence that the lesions are disseminated not only in space (ie.,in different locations) but in time (symptoms or signs should develop at different times).
The diagnosis remains essentially a clinical one, based on symptoms and signs of the individual's Nervous System malfunction.
A symptom is something that is reported by the patient. A sign is an abnormality detected by the physican while examining the person. At times signs confirm the presence of symptoms.
Some abnormal reflexes or loss of Vibratory Sense may be present without the patient being aware of anything being wrong. Symptoms are subjective complaints, whereas signs are objective observations.
It must be emphasized that lesions that do not produce any symptom or even signs of malfunction, exist in practically every MSer.
It is important to realize this, so that the appearance of a new symptom does not necessarily signify the formation of a new lesion.
It is difficult to understand how lesions that are discovered at autopsy have not produced symptoms in view of their location and size, but they are seen repeatedly.