No, Toll-like receptor cannot be an antigen. I fail to understand in what context have you asked the above question, but I hope the following explanation may help.
Toll-like receptors (TLRs) are components of the innate immune system that respond to exogenous infectious ligands (pathogen-associated molecular patterns, PAMPs) and endogenous molecules that are released during host tissue injury/death (damage-associated molecular patterns, DAMPs). TLRs were previously believed to only be expressed in immune cells. But they have now been found to be ubiquitously expressed in cells within the body including neurons, astrocytes, and microglia of the central nervous system (CNS).
Most DAMPs are sequestered from the immune response. However, during CNS infection and disease, self-antigens and/or danger signals may be liberated as a consequence of cell death, necrosis, or tissue remodeling. The expression of TLRs and related signaling proteins has been demonstrated in all major glial cell types, including microglia, astrocytes, and oligodendrocytes as well as a more limited repertoire in neurons. Thus, TLR engagement may be elicited by a combination of PAMPs and/or DAMPs during inflammatory CNS disorders.
For instance, inflammation plays an important role in Alzheimer's disease (AD). The innate immune system may primarily act as defence mechanism, misinterpreting the misfolded and aggregated Aβ species as bacterial surfaces and therefore as DAMPs. Neurons and glial cells, which have been equipped with numerous Pattern Recognition Receptors (PRRs), react to Aβ and drive immune pathway activation. An increasing expression of inflammatory mediators and the subsequent release of further DAMPs seem able to establish a vicious cycle and sustain brain inflammation. DAMPs activate TLRs and their coreceptors, creating an oxidative and neuroinflammatory environment in AD via excessive production and release of proinflammatory cytokines, ROS and NO.
You may want to refer to the article attached below.
Article Danger-associated molecular patterns in Alzheimers disease
An antigen is something that you have an adaptive immune response against. If you had an autoimmunity against your own Toll-like receptor then the TLR would be the antigen.
It IS an antigen, a self-antigen. As a species, we have evolved not to react to it, therefore it is not immunogenic for us. The molecular integrity of a TLR would have to be modified (via mutation, haptenation, or other events) as to be recognized by the immune system as foreign and mounting a response (T-cells, antibodies) against it.
On the other hand, injecting a (purified) human TLR into another animal would elicit an immune response as it would be a foreign molecule. As you can see, whether or not TRL can act as an immunogenic antigen (immunogen) completely depends on the context.