Graves’ ophthalmopathy, also known as thyroid eye disease (TED), is an autoimmune inflammatory disorder of the orbit and periorbital tissues, characterized by upper eyelid retraction, lid lag, swelling, redness (erythema), conjunctivitis, and bulging eyes (exophthalmos). It occurs most commonly in individuals with Graves disease, and less commonly in individuals with Hashimotos thyroiditis, or in those who are euthyroid.It is part of a systemic process with variable expression in the eyes, thyroid, and skin, caused by autoantibodies that bind to tissues in those organs. The autoantibodies target the fibroblasts in the eye muscles, and those fibroblasts can differentiate into fat cells (adipocytes). Fat cells and muscles expand and become inflamed. Veins become compressed and are unable to drain fluid, causing edema.Annual incidence is 16/100,000 in women, 3/100,000 in men. About 3–5% have severe disease with intense pain, and sight-threatening corneal ulceration or compression of the optic nerve. Cigarette smoking, which is associated with many autoimmune diseases, raises the incidence 7.7-fold.Mild disease will often resolve and merely requires measures to reduce discomfort and dryness, such as artificial tears and smoking cessation if possible. Severe cases are a medical emergency, and are treated with glucocorticoids (steroids), and sometimes ciclosporin. Many anti-inflammatory biological mediators, such as infliximab, etanercept, and anakinra are being tried. In January 2020, the US Food and Drug Administration approved teprotumumab-trbw for the treatment of Graves’ ophthalmopathy. Signs and symptoms
In mild disease,  patients present with eyelid retraction. In fact, upper eyelid retraction is the most common ocular sign of Graves orbitopathy.
Nezelof syndrome is an autosomal recessive congenital immunodeficiency condition due to underdevelopment of the thymus. The defect is a type of purine nucleoside phosphorylase deficiency with inactive phosphorylase, this results in an accumulation of deoxy-GTP which inhibits ribonucleotide reductase. Ribonucleotide reductase catalyzes the formation of deoxyribonucleotides from ribonucleotides, thus, DNA replication is inhibited. Symptoms and signs
This condition causes severe infections. it is characterized by elevated immunoglobulins that function poorly. Other symptoms are:
Bronchiectasis
Hepatosplenomegaly
Pyoderma
Emphysema
Diarrhea

Cause
Genetically speaking, Nezelof syndrome is autosomal recessive. the condition is thought to be a variation of severe combined immunodeficiency (SCID). However, the precise cause of Nezelof syndrome remains uncertain

Mechanism
In the mechanism of this condition, one first finds that the normal function of the thymus has it being important in T-cell development and release into the bodys blood circulation Hassals corpuscles absence in thymus(atrophy) has an effect on T-cells. Diagnosis
The diagnosis of Nezelof syndrome will indicate a deficiency of T-cells, additionally in ascertaining the condition the following is done:
Blood test (B-cells will be normal)
X-ray of thymus (atrophy present)

Differential diagnosis
The differential diagnosis for this condition consists of acquired immune deficiency syndrome and severe combined immunodeficiency syndrome

Treatment
In terms of treatment for individuals with Nezelof syndrome, which was first  characterized in 1964, includes the following(how effective bone marrow transplant is uncertain) :

Antimicrobial therapy
IV immunoglobulin
Bone marrow transplantation
Thymus transplantation
Thymus factors

See also
List of radiographic findings associated with cutaneous conditions

References
Further reading
Lavini, Corrado; Moran, Cesar A.; Uliano, Morandi; Schoenhuber, Rudolf (2009-05-08). Thymus Gland Pathology: Clinical, Diagnostic and Therapeutic Features. Springer Science & Business Media. ISBN 9788847008281. External links
PubMed