IMMUNOLOGY TEXTBOOK - Mercury Podillia 2013
MECHANISMS OF IMMUNE DEFENSE IN BACTERIAL, VIRAL, FUNGAL, AND PROTOZOAN INFECTIONS
Features of Immune Status in Autoimmune Diseases
When evaluating the characteristics of an immunogram in autoimmune diseases, the TYPES OF IMMUNE response must be taken into account. For a practicing physician, the value of the analysis lies in identifying the specific type of immune disorder and prescribing appropriate therapy. Even in the presence of clinical guidelines, Treatment should be tailored to the Immune Response types of the individual patient. Thus, based on the predominance of immune response types, most autoimmune diseases can be divided into the following groups (Table 41).
Class="center">Table 41. Types of Immune Response According to Autoimmune Diseases
Th1>Th2 Predominance |
Th2 Activation Only |
Th2>Th1 Predominance |
Rheumatoid Arthritis |
Systemic lupus erythematosus |
|
Lyme arthritis |
Churg-Strauss syndrome |
Systemic lupus erythematosus |
Juvenile chronic arthritis |
||
Wegener's granulomatosis |
Systemic sclerosis |
|
Giant Cell arteritis |
Sjögren's syndrome |
|
Considering the Classification of immunological tissue damage types (according to Gell and Coombs), it should be noted that autoimmune diseases are typically characterized by inflammation of a cytotoxic or immune-complex nature.
Most commonly, the following immune status disorders can be detected in an autoimmune process:
✵ The Development of an autoimmune process involves The production of autoantibodies, The formation of A large number of circulating immune complexes (CICs), and/or the activation of lymphocytes (sensitized to self-tissue Antigens). The damaging effect of CICs is due to their deposition in Tissues, leading to local phagocytosis activation, Complement system activation, or direct lymphocyte-mediated damage;
✵ common indicators of an ongoing autoimmune process may include: lymphomonocytosis, elevated lymphocyte counts, increased levels of complement system Proteins (CH50), circulating immune complexes (CICs, especially small-sized ones), IMMUNOGLOBULINS of classes G and M, and increased neutrophil phagocytic activity (PI, PA)—predominantly in the cytotoxic type of autoimmune reactions;
✵ in the immune-complex type of damage, non-specific defense factors (The Complement System) are triggered, which is why the immune profile is typically characterized by decreased CIC levels and low hemolytic activity of complement (CH50);
✵ it should be noted that during an acute process, quantitative parameters may appear decreased due to CIC deposition or consumption of complement proteins, whereas during remission or as the acute phase subsides, these levels increase significantly. Thus, depressed CIC levels do not automatically rule out an autoimmune disease;
✵ regarding specific immunodiagnostics for autoimmune diseases (detection of specific autoantibodies, measurement of interleukins, TNF-alpha), these Methods reveal the body's sensitization (predisposition) to an autoimmune process and its actual presence, but they do not answer the question of what stage the disease is in or what its current activity level is.
As an example of immune system dysfunction in the presence of an autoimmune disease, consider the medical history of patient O., 47 years old, suffering from rheumatoid arthritis with involvement of the interphalangeal and metacarpophalangeal JOINTS OF THE hands and metatarsophalangeal joints of the feet, seropositive (RF+), severe course, moderately severe exacerbation. Granulocytic-type immune system dysfunction, quantitative T-cell deficiency. High C-reactive protein levels, elevated RF.
Immunogram Conclusion. Decreased Hemoglobin and erythrocyte levels, high ESR, absolute leukopenia. High neutrophil phagocytic activity (PI, PA), reduced functional reserve of the oxidation-reduction potential (NBT res.). High C-reactive protein levels, elevated RF. The patient demonstrated elevated levels of circulating immune complexes (CICs) and immunoglobulins classes G and A. Decreased absolute T-lymphocyte count (CD3) and their functional activity (LST) (Table 42).
Diagnosis: rheumatoid arthritis with involvement of the interphalangeal and metacarpophalangeal joints of the hands and metatarsophalangeal joints of the feet, seropositive (RF+), severe course, moderately severe exacerbation. Granulocytic-type immune system dysfunction, quantitative T-cell deficiency.
Conclusion: anemia, leukopenia, signs of an acute inflammatory process with elevated acute-phase proteins (APPs), CICs, dysimmunoglobulinemia, neutrophil dysregulation, quantitative T-cell deficiency; autoimmune diseases, space-occupying lesions, and viral infections (HIV, HCV) should be ruled out.
Based on the immunological status characteristics of patient O., 47 years old, the following therapy regimen has been prescribed for etiotropic treatment and immunological correction of the clinical manifestations of her severe rheumatoid arthritis:
1) Rituximab (MabThera) 500 mg every 2 weeks intravenous infusion for 6 weeks; initial infusion rate for the first dose 50 mg/h, with a gradual increase of 50 mg/h every 30 min (maximum rate 400 mg/h). The interval between repeat courses is 12 months.
Blood cell counts must be monitored at least once a month, and CRP, RF, and immunogram concentrations at least 4 times a year.
Table 42. Immunogram of Patient O., 47 Years Old
Parameter |
Result |
Reference Range |
||||||
Hemoglobin |
107 |
F - 115 - 145, M - 132 - 164 g/L |
||||||
Erythrocytes |
3.2 |
F - 3.7 - 4.7, M - 4.0 - 5.1x1012/L |
||||||
Platelets |
170 |
150 - 320x109/L |
||||||
ESR |
69 |
2 - 15 mm/h |
||||||
Leukocytes |
3.3 |
4 - 9x109/L |
||||||
Neutr. |
Band |
Seg. |
Eosin. |
Baso. |
Mono. |
LGL |
Plasma |
|
43 - 71 % |
1 - 4 % |
0.5 - 5% |
0 - 1% |
3 - 9% |
25 - 37% |
1-5% |
0 - 1% |
|
2000-6500 |
80-400 |
80-370 |
20-80 |
90-720 |
1600-3000 |
80-500 |
20-80 |
|
63 |
5 |
58 |
3 |
1 |
7 |
26 |
0 |
0 |
1950 |
160 |
1800 |
100 |
30 |
220 |
810 |
0 |
0 |
Immunological Parameters |
Result |
Reference |
Immunological Parameters |
Result |
Reference |
|||
(SI Units) |
(SI Units) |
|||||||
T-lymph. |
% |
52 |
50 - 80 |
Ig G |
23.66 |
8.0-18.0 |
||
CD-3 |
Abs. count |
420 |
1000-2200 |
g/L |
||||
T-helper |
% |
29 |
33-46 |
Ig M |
1.06 |
0.2-2.0 g/L |
||
CD-4 |
Abs. count |
230 |
309-1571 |
|||||
T-suppr. |
% |
20 |
17-30 |
Ig A |
5.38 |
0.3-3.0 g/L |
||
CD-8 |
Abs. count |
162 |
282-999 |
|||||
IRI |
CD-4/CD-8 |
1.45 |
1.4-2.0 |
CIC |
104 |
30 - 50 Units |
||
opt. dens. |
||||||||
NK Cells CD-16 |
% |
23 |
12 - 23 |
Phagocytic |
PA |
91 |
60 - 80% |
|
Abs. count |
186 |
72-543 |
activity |
PI |
5.04 |
1.5 - 3.5 |
||
B-lymph. |
% |
16 |
17-31 |
NBT test |
spon. |
3 |
up to 10% |
|
CD-22 |
Abs. count |
129 |
109-532 |
ind. |
14 |
- |
||
LST |
spon. |
3 |
up to 10% |
res. |
11 |
h16% |
||
ind. |
35 |
50-70% |
Complement |
CH-50 |
42 |
30 - 60 |
||
hem. U/mL |
||||||||
CRP |
96 |
<6 mg/L |
||||||
RF |
120 |
<12 IU/L |
||||||
ASO |
- |
<200 IU/L |
||||||
Last update: 13/08/2026
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